text:
Lateral corticospinal tract and termination
I'm studying the motor pathways of the brain and I'm a bit confused about how the lateral corticospinal tract descends.
From Neuroanatomy: Text and Atlas by Martin, J. H., 4th edition, right before Figure 10-4:

Some of these [terminating] axons descend ipsilaterally; many descend
  contra-laterally and re-cross midline within the gray matter in lamina 10.
  The function of these ipsilateral axons is not well understood.

I understand that the axons cross over at the Pyramidal decussation, but this paragraph is really confusing me. What descent is being referenced here? Is it descending in the spinal chord? Alternatively, is the paragraph implying that some axons don't decussate in the pyramidal decussation?

Can you provide a page number and tell us what edition of Martin you're using?

@Susan Fixed. Unfortunately, I can't give you a page number because I'm using the Kindle edition of the textbook. I tried to give the most accurate reference I could.

The answer ends up being on the next page when discussing the ventral corticospinal tract.

Many ventral corticospinal tract axons have branches that decussate in
  the spinal cord, similar to the re-crossed lateral coticospinal tract
  axons described earlier.

In other words, some axons of the lateral corticospinal tract ignore the pyramidal decussation, join the anterior corticospinal tract (which then synapses bilaterally later at the spinal commissure).


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

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

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Molecular Evolution: Mrbayes never stops?
When I use my own data to build Bayesian phylogenetic trees using the software Mrbayes, after many generations, it never reaches stopping status (namely, the average standard deviation of split frequencies below 0.01).
What should I do to get to this point?
The dtype is protein, 37 taxa were included, the model I used was as follows:
prset aamodel=fixed(wag);
lset rates=Invgamma;
mcmc ngen=100000 samplefreq=100

There are a few things you can try to get better convergence. I'd try the following in increasing order of difficulty/effort/processing time.

Be satisfied with a higher standard deviation of split frequencies. The MrBayes manual says "A rough guide is that an average standard deviation below 0.01 is very good indication of convergence, while values between 0.01 and 0.05 may be adequate depending on the purpose of your analysis." Especially if you are interested only in the best supported parts of the tree, this is a viable option. 0.01 is only a guideline.
Run the model for more generations. Maybe it is on the way to converging, but it hasn't gotten there yet. 100000 is not really that many. Try 200000 or 500000 and see if the model space is still being explored. You can examine the .p files using Tracer. You may already be doing this, and this is why you know it is not converging. If you look at the plots of the log-likelihoods, they will become relatively stable when the run has reached the optimal location.
Try running with a different amino acid model or without the inverse gamma rate prior. If you can get a simpler model to converge, then
Increase the number of chains to 4 or 8. If you have the ability to run in parallel, this will greatly speed up your analyses.
Try iteratively changing the heating parameter by setting Temp to a lower value, which will increase the likelihood of a swap. By default, Temp = 0.1. You can watch the progress of the analysis in the command line and see which are the heated chains and which is the cold chain.

Many thanks, kmm! These are very useful suggestions, and with these information, I really got good results. There is also another question: the model I selected was based on the results of model test program ProtTest, so although it is difficult to converge, is it the right way to choose a simple model for the analysis? (I mean this operation will produce good results, but the results may be controversal.)

And if all what kmm suggests fail, it may be time to fiddle with finer tunings, such as concerning the proposals that are used to modify the Markov chain.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
What is the name of the critter depicted in the attached image?
I found a critter on my bathroom towel. It's really tiny. Maybe 2 milimetres? I placed it on an envelope for the photograph.
Can someone identify what it is?

Possible duplicate of Bug Identification: Is this small tubular, black bug a bed bug?

Related: What kind of insect can this be?..., Can anyone help confirm this tiny insect larvae?, Bug Identification: Is this small tubular, black bug...,
How to protect my mounted insect specimens..., Varied Carpet Beetle Larvae, What small insect is this?, What bug is this...

That is the larva of a carpet beetle.

Larvae feed on natural fibers and can damage carpets, furniture, clothing and insect collections.

"Anthrenus verbasci - larva side (aka)" by André Karwath aka Aka on Wikimedia
Related question: What kind of caterpillar is this?, though I think that the larva photographed in that example is either of a different species or at a different time period within the larval stage.

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


text:
Does the tannin level in plants go down or up after they die? Or does the tannin level stay the same regardless?
Does the tannin level in plants go down or up after they die? Or does the tannin level stay the same regardless?
As they decay, do they release more tannins or does the production stop?

What do you mean about go down/up?

Well maybe I'm confused, but do plants not produce tannins? If they do does the production of the tannins stop after death? Does the level of tannic acid decay as the plan dies/Decays?

Well maybe I'm confused, but do plants not produce tannins? If they do
  does the production of the tannins stop after death?

That depends on how you define death. Tannin is secondary product, so I don't think the plant cells will produce more tannin when they are starving probably because of cutting off the leaves, roots, etc... when the plant dies. The plant won't bother to degrade tannins (I guess it does not even have the pathway necessary to do that), because it is a defense mechanism against insects, mammalians, etc... and not an energy storage material. Tannins can be degraded by microbes, heat, UV radiation, chemical reactions, etc... So if you can't protect the tannins from all of these then they will degrade. (Note: you can't, all you can do is slowing down the process.)

Exactly, what I was looking for. I wasn't sure exactly what would happen as a plant dies or ages. So tannins are like an inevitable process of ageing, you can't stop the Loss but you can delay the process.

@user3061879 I don't think tannins have anything to do with aging. It is for protection against animals. They have a decay rate, so the plant has to produce them life long. Producing tannins is costly, so many plant produce less tannins and rebuild leaves faster, so the amount of tannins depends on the species. http://link.springer.com/article/10.1007/BF00380050#page-1


text:
How many eukaryotes are there on Earth?
I have been reading:

William B. Whitman, David C. Coleman, and William J. Wiebe, "Prokaryotes: The unseen majority", Proc. Natl. Acad. Sci. USA 95, pp. 6578–6583, June 1998.  [Full Text] [PDF]

wherein they estimate the number of prokaryote cells on Earth to be of the order of $10^{31}$.
I can't seem to find any equivalent data for eukaryote one-celled life. Are there any estimates for the number of one-celled eukaryotic living things on Earth? Do any other estimates confirm or tell against the reference I have cited above?

Could not fit in a comment....
To make sure we all understand your question...
Is your question how many (eukaryote) species are currently living? or How many (eukaryote) cells are currently living??
Just a hint to answer the question
Micheal Lynch, in his book (On the Origin of Genome Architecture) at page 3, Box 1.1 tries to answer the question How much DNA is there on earth?. He ends up with an estimation of a total length of DNA on earth of $10^{24}$ km for procaryotes, $10^{25}$ km for eukaryote (of which $\frac{1}{1000}$% is accounted to humans). This sums up to a total DNA length of $10^{12}$ light-years, or 10 times the diameter of the known universe!
In his calculations, he estimates that the total number of procaryote cells at $10^{30}$ (citing Whitman et al. 1998 as you did). He estimates the total number of eukaryote species to $10^7$, i.e. 6 times the number of known eukaryote species. However, he doesn't directly give any reference for this estimate but he refers to different chapters in the book that contain lots of references.
...I hope that helps...

"How many eukaryotes cells are currently living?? or How many eukaryotes cells are currently living??" It's how many cells are currently living, so your reference is indeed helpful, thanks.


text:
Is it possible to get infected with HIV from old blood?
Let's say that someone uses a needle which has some old blood infected with HIV. In this case, is it possible for them to get infected with HIV?

Doesn't the oxygen of air eliminate the virus?

It's important to define how old is "old", here, I think.  I rephrased the question a bit so that it focuses more on the science than an individual diagnosis.

Thanks. Let's not define old in order to have a complete answer. I suppose the answer is based on that.

Yes, you can transmit HIV with infected needles/syringes. This is a quite common mechanism of transmission when drug addicts share and re-use needles and syringes and also in third world hospitals with poor hygiene standards.
A drop of blood is considered infectious at least until it has completely dried up (some research showed that it might be contagious for up to 5 days longer when the conditions are right, see reference 1 below). Mostly HIV is senstive against high temperatures (over 60°C), while it is stable at low temperatures. It is very sensitive against shifts in pH (below 7 or above 8) and also against desinfectants like bleach. Have a look at the references below, a lot of research has been done by Abdala et al. in this field. You can find his whole reference list here (it contains more articles in this field).

References:

Survival of HIV-1 activity after disinfection, temperature and pH
changes, or drying.
Survival of HIV-1 in syringes.
Survival of HIV-1 in syringes: effects of temperature during
storage.
Viability of HIV-1 in syringes: implications for interventions among
injection drug users.


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

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

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

There is no way currently to tell us the exact meaning of the genetic code; Ask this question in 30 years and you may have the answer. AFAIK it is based off the environment as even different environments cause epigenetic changes in the expression of genes,

Yes, there is a biological basis. Your examples seem a little social/cultural to me, though. In any case, here are some examples I came across. One study that showed that women's hormones rose in response to smelling male sweat.  There's also a large psychological component that, for example, shows people find symmetry important in beauty.
A review discusses various aspects of facial beauty, and mentions that several studies have shown certain physical attractiveness standards are common across ethnic groups. It also mentions another study that shows how women are more attracted to a "masculine" face during the high-risk phase of their menstrual cycle.

Just to clarify, there are cultural biases as to what traits are attractive at the moment or given your own genetic make up when the specific traits mentioned in the question are considered.

@shigeta I agree, and I didn't mean it to sound like attraction was completely biological, just that there is some biological part of it. The examples I chose (or at least the first and last ones) were intended to highlight interesting and bizarre findings that caught my attention. I wrote it at work, so I probably didn't do a good job of writing it up...

i like your answer - just wanted to add a footnote... sometimes when I am abroad I'm struck by how movie stars we might view as 'on the chunky side' are the biggest hits there....


text:
Does the human ear adapt to noise levels?
I have noticed lately that if I go to sleep, when I have my radio running, it is on lowest volume, I still consider it kind of loud.
In the morning, when being on the edge of waking up, I hear the birds, and the tennis balls already being batted on the court nearby, but I do not hear my radio. If I wait a few more minutes, I start to hear the radio, with no changes in the sound levels outside.
I know that the human eye adapts to the light levels (aperture, what cells used), but is there something similar for sound sensitivity?
Note, the radio is on that occasion running all night long, with always the same sound level.

In  this instance, I would say your attention has been adjusted, not your ear's ability to perceive sound. Our ears don't have a control setting or a means of adjusting incoming sound levels (though I'm certain when an ambulance with loud siren drives by, we all wish we did).
What you are experiencing is a prioritization of the sound by your brain in relationship to other sounds.

You put the sound on before you go to sleep. Your brain accepts that incoming sound as non-vital, non-threatening sound. (Radio, meant to soothe, supposed to be there, relegate this sound to innocuous)
Come dawn, new and novel sounds appear. For our brains, the new and novel could indicate a threat, so your brain prioritizes that sound over the known and considered innocuous sound (your radio) which it has heard all night. Birds, tennis balls on courts are distinctive enough your brain would prioritize them even though you know in your conscious mind neither is an actual threat.
As you waken, your brain then reminds you there is still another sound in your environment which is not threatening and yet still prevalent (your radio) prompting you to decide if you want to do anything with the non-threatening sound.

Yes, this is an oversimplification of a very complex process of sound prioritization but most modern science bears this out. As a curiosity, our minds are predisposed to seek out information which may be vital to us, hence the reason conversations held by other people who are on the phone are so distracting because our brains dislike hearing things which may be necessary to our survival but only hearing half of the conversation.
EDIT:
As I was reminded there are some involuntary control elements built into the ear via:

the tensor tympani muscle whose role is to dampen sounds (mainly internal ones such as chewing)
and the stapedius muscle which dampens the ability of the stapes vibration and protects the inner ear from high noise levels, primarily the volume of your own voice.

You can thank the stapedius muscle for making your voice sound so strange to you when you hear it on a recording. You have never truly heard your voice until you hear an external recording and playback of it!

Although I think you are correct about prioritization as the reason behind the described phenomenon, I disagree that "Our ears don't have a control setting or a means of adjusting incoming sound levels". The tensor tympani and stapedius both help attenuate the mechanical response to loud sounds.

Then perhaps the word I should have used was a "conscious" and controllable ability to regulate unwanted sound...I would be completely deaf when my son starts his thrash metal music with the dial at 11...


text:
Beginner question about growing E. coli
I have bought a hobbyist kit which involves growing E. coli. The steps said to grow the E. coli on an LB agar Petri dish overnight. No incubation devices were included in the kit.
I let the E. coli grow overnight at room temperature (65-75°F), but there's pretty minimal growth, if any. I found this question which seems to imply that it's hard to grow E. coli without having temperatures near 37°C, which is much warmer than I can reasonably make my house.
Is it possible for me to do this experiment without purchasing an incubator of some sort? If so, does the lack of growth indicate that I've made a mistake somewhere?

You can always put the plates close to the heating source for your house - forced hot air vents, baseboard electric or hot water heaters, radiators, etc. (I'm assuming you're in the Northern hemisphere and you have the heat turned on). It will be several to many degrees warmer there than in the rest of the room. Make sure you place a good thermometer at exactly the distance away from the heat source that you'll be putting the plate(s) so you don't cook them accidentally - steam radiators, for example, get really hot.

The higher the temperature the faster E. coli will grow, with a maximum growth rate around 37 Celsius.
If you grow E coli at lower temperature, the ecoli will grow slower.
At 37°C you will see colonies overnight (16hr).
At 30°C you will see colonies in about 1 and a half days.
At 25°C you will see colonies in about 3-4 days.
You can do experiments at room temperature, but you will be waiting for days for what you will normally see after a 37°C overnight incubation.
As for satellite colonies.. yes ampicilin does break down with time and water. You can solve that problem by increasing the amount of Amp you are using from 25ug/ml to 100ug/ml. Or use 75ug/ml Carbenicilin. Or change your selection markers and use a more stable antibiotic like Chloroamphenicol.

Pedantic stuff: Overnight is typically 8-9 hours and the colony growth rate also depends on the concentration of the inoculum.

@WYSIWYG Your overnight is 8-9 hours? What are your lab hours? Mine is at least 16h.

@MattDMo 16h is your lab hours?!! I guess not, unless you are a robot :D I guess you meant "overnight". My lab hours are variable (as less as 3h to max 15h) :P Recently I was doing only computational; so I could fire commands from anywhere. When I was doing experimental then lab hours were on an average ~10h; 10 AM to 8 PM. All my "overnight" inoculations are done at ~9 PM (but later the better) and I harvest the cells in the morning ASAP. For maxipreps I inoculate late and harvest in 9-10h. Overgrown cells give bad preps.

@WYSIWYG sorry, I meant my "overnight" is about 16-ish hours. I work in industry, so 9AM-5PM is the norm :) It's been a few years since I've done plasmid preps, but I can't recall having any issues with the longer incubation time. YMMV, of course.

@MattDMo There are no big issues but the cell lysis doesn't happen properly when the cells are overgrown. The lysate is very sticky and viscous. The yield goes down.

@WYSIWYG If we're being pedantic, then 8-9h as an overnight incubation definitely isn't "typical" :P that's overday if anything.


text:
Why does the chance of having a baby with Down's syndrome increase with the age of the mother?
Down's syndrome occurs when either the egg or the sperm cell contain on extra chromosome 21. To my understanding, women are born with all the egg cells in place already, so there's no further cell divisions, and thus no further chance of having one cell with an extra chromosome.
Now, the chance of having a baby with Down's syndrome increase with age:

At maternal age 20 to 24, the probability is one in 1562; at age 35 to 39 the probability is one in 214, and above age 45 the probability is one in 19

Why is this so, when the egg cells are complete at birth?

It is true that woman are born with all the eggs they will ever release , meiosis is not completed in the egg. There will be a meiotic cell division. Now this might sound confusing to you how there can be cell division without increase of egg number. For this - I will recommend that you read any basic bio textbook covering both the meiosis and gamete formation in females.

I think by this discussion it is clear that there is a chance of having one cell with extra chromosome.

The frequency rises with maternal age due to a peculiarity of meoisis
  in female mammals.  Meiosis is originated in the fetal ovary,
  arresting at metaphase I with the homologous  chromosomes aligned for
  segregation. Cells remain in this state until the time of ovulation,
  often  decades later in humans. The longer cells remain in the
  arrested state, the greater the chance  that there will be a
  nondisjunction event when meiosis resumes.

Source : http://www.madsci.org/posts/archives/2005-07/1121714807.Ge.r.html
I think you have the misconception that egg cells have completed meiosis by the time female is born. This is not true ( as indicated above in the answer). At birth, they are in metaphase I , after puberty, each month some of them divide further but only one survives and get arrested at metaphase II . Only after fertilization is the meiosis complete.

If you are not familiar with some of the terms or have any other confusion , ask !

If you expect folks may have difficulties with jargon, linking appropriate pages in your answer may help. Great answer here btw +1

no need to be careful! Just a hint :)

It isn't right that in Metaphase-I oogenesis gets arrested until puberty but actually in diplotene stage. The secondary oocyte after having completed Meiosis-I enters Meiosis-II and gets arrested in Metaphase-II until fertilisation(not syngamy). Source Besides madsci.org is not a reliable source, it's a Q&A site.

@biogirl Even I was wondering this for a long time then. Very fluid, biogirl. PS: just checked your bio(profile) and it seems(seemed) to me like I was reading something that I had written long back. Akin :) kudos and best of luck to your future endeavours. Sorry for this redundant praise incase if it doesn't fit in here but take my kudos ;)

@biogirl I would like to add 1 thing I think primary oocytes get arrested at prophase -1  of meiosis and stays in this state till puberty,  after ovulation begins in ,it gets arrested at metaphase-2 until it gets fertilized by sperm

The chance of having a child with Down's Syndrome does not only have to do with cell division, but the mechanism that allows spontaneous abortion to occur within the uterus of the mother.

There is strong evidence for uterine selection against genetically disadvantaged embryos.  However, as women approach the menopause and the risk of future infertility increases, this selection, or filtering stringency, is expected to relax.
Neuhäuser and Krackow’s paper provides evidence that older mothers, who give birth to children with Down Syndrome, have a relaxed stringency of quality control of embryos (or relaxed filtering stringency), which increases the probability that these women will bring children with developmental defects to full term.  They believe that this relaxed filtering stringency is an adaptive maternal response and it might explain why the rate of Down Syndrome accelerates with increasing maternal age.

Basically, the mechanism that allows for the uterus to select against 'genetically disadvantaged embryos' (which can be Down's Syndrome, or other genetic deficiencies) is not as good at detecting these problems, OR as this paper suggests, is 'less picky' about the genetic quality of the fertilized egg, and will allow it to implant in the uterine walls.
It is also important to note that these studies are all ongoing, and many different reasons for the development of Down's Syndrome are unknown.
Literature Cited
Neuhäuser M & Krackow S (2006).  Adaptive-filtering of trisomy 21: risk of Down Syndrome depends on family size and age of previous child.  (Naturwissenschaften, DOI 10.1007/s00114-006-0165-3)

That's a very interesting finding. Are there any models for relaxed filtering stringency (RFS) in animal models?


text:
If someone were to die on the moon, would their body decay?
I heard that the footprints of Neil Armstrong are still there, so I was wondering if someone were to die there, would they remain preserved, too?
If not how long would it take for them to decay?

i think this question suits more for skeptics.se

why? don't you believe in decay Agha?

Are you asking about if an astronaut died in their spacesuit or an unprotected body?

@shigeta.. I don't think it is opinion based... It is answerable but clearly there is no effort shown in the question. I consider this a homework.

@WYSIWYG I know what you mean,  Just hoping stronger users like yourself can help the newer users with edits.... good writing is hard and its particularly hard in science. On the other hand science is in need of stronger public relations.

Related questions on Space Exploration: http://space.stackexchange.com/q/5666/5963, http://space.stackexchange.com/q/308/5963

I am assuming in spacesuit here, on the face (lit side) of the moon. Bodily degradation involves much more than external fungi and bacteria.
Cells that receive no oxygen or nutrients die. We talk of such tissue death as dry gangrene when it affects extremities, such as fingers, feet, etc. However, we also recognize gangrenous bowel, etc. which results in tissue necrosis.
Such necrotic cell death is the consequence of acute disruption of cellular metabolism, leading to ATP depletion, ion dysregulation, mitochondrial and cellular swelling, activation of degradative enzymes, plasma membrane failure and cell lysis [1]
Lysis is messy and wet. Combined with the fluids in our bodies, what one would end up with is a mushy, smelly degraded body, not a preserved body. For a while, anaerobic bowel bacteria would flourish (which smell terrible).
Add to this the extremes of temperature (253° F in the sun and -243° F in the dark.) The suit would have lost it's heating and cooling mechanisms, so the body would alternately spend 14 days in the heat and 14 days in the freezing cold depending exactly where it was (lets say the equator of the moon.) These freeze/bake cycles would further contribute to degradation through ice crystal formation and thawing.
Eventually, because there was no new substrate, degradation would come to a halt, but I'm not sure at what stage this would be. I assume, though, there would be a vast difference between a mummified body (done by dehydration) and a body left to degrade in a spacesuit.
[1] The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy, John J. Lemasters et. al, Biochimica et Biophysica Acta 1366 (1998) 177-196

I wonder if the body would 'pop' the spacesuit by putting too much pressure on the suit by boiling in the heat. What does a partially decayed then autoclaved body look like?

@Resonating - Space suit as pressure cooker. :-O

Decay is a process where the body is digested by bacteria, fungi and other living things.
The moon has no known biological processes and while its possible for some microorganisms to survive in space, I think its generally understood that the lunar surface would not support life in a significant way, especially if the body is in vacuum.
Other processes would definitely take place. Mummification can result from the body dehydrating and direct exposure to solar radiation will also break down the corpse, but it will mostly leave the body intact.

So, essentially no but to some extent yes? :)

so essentially no :)  mummification is more of a form of preservation, as opposed to decay

I think the body would undergo decay. While it is true that the moon does not contain living organisms capable of decaying a dead human body, the human body itself contains huge load of bacteria→ on skin surface and gut which will continue to grow.
The aerobic bacteria will die out as soon as oxygen is removed which is very soon. The anaerobic bacteria will continue to grow and proliferate till substrate (dead human body) will cease to exist. This will be regulated as anongoodnurse has pointed out by the heat and light.
Further, the infectious status of the dead person will also matter. Any fungal infection can alter the rate of decay.


text:
How many smaller muscles compose the interosseus muscle in the human hand?
When looking at Wikipedia, I read that the interosseus muscle is actually composed of 3 muscles, but on the French Wikipedia, they talk about a 4th muscle.
So how many interosseus muscle components are there, 3 or 4?

The number of interosseous muscles is not constant, because of the evolutional process continuing in modern generations.
Some individuals have 4 interosseous muscles, other have three, however there are still debates about the subject:

+


text:
Where does the term "cos site" come from?
The word cosmid is derived from cos sites of lambda phages.
Why are cos sites called cos sites? What does this "cos" refer to?

"Cos" is the abbreviation of "cohesive end site". This is a speciality of the lambda phage which has to be linearized to fit into the phages head, but circularizes in the host cell. To achieve this, it has the cohesive (or sticky) sites at each end.
See here and also the publication by Allan Campbell on "Bacteriophages".

The 12 bp overlapping sticky ends at the termini of pure lambda DNA are generated during DNA packaging. Another term for this complementary base-pairing is "cohesive" and so cos is an abbreviation of that term. I believe it was italicized because it could also be mapped genetically. Scott Emmons is credited with coining this term (and using it first) when he was a grad student at Stanford.

Cos is for "cohesive," as in these sites rather easily recircularize the linear phage DNA through complementary base-pairing (they're sticky ends, generally G-C rich). See Wikipedia.

The term cos comes from its originator Dr. Scott Emmons.  He coined it by using "co" from the word cohesive and "s" from the word site (cohesive ends site).  He was going to use ces (for cohesive ends site), but decided the term ces was suggestive of sanitary waste.


text:
What is the exact chemical composition of human body?
I've just watched Breaking Bad Season 01 Episode 03. In that Walter gives the chemical composition of human body. The conversation is as follows

Walter White: Let's break it down. Hydrogen. What does that give us?
Gretchen Schwartz: We're looking at 63%.
Walter White: Sixty-three, that is a big bite. My next step's gotta be
  oxygen.
Gretchen Schwartz: Oxygen, 26%.
Walter White: Twenty-six. There you have your water.
Gretchen Schwartz: Carbon, 9%.
Walter White: Carbon, 9.
Gretchen Schwartz: For a total of 98%.
Walter White: Right.
Gretchen Schwartz: Nitrogen, 1.25%.
Walter White: One-point-two-five.
Gretchen Schwartz: That brings you to 99 and a quarter. Which only
  leaves you with the trace elements down where the magic happens.
Walter White: Oh, wait a minute. What about calcium? Calcium's not a
  trace. Got a whole skeleton to account for.
Gretchen Schwartz: You would think, right? Calcium's only 0.25%.
Walter White: What? That low? Seriously? Damn, I never would've
  thought that. Okay, so where does iron fit in.
Gretchen Schwartz: Iron. 0.00004%
Walter White: What? You can't have hemoglobin without iron.
Gretchen Schwartz: Apparently, it don't take take much. No doubt. Go
  figure.
Walter White: Sodium.
Gretchen Schwartz: Sodium, 0.04%. Phosphorus, 0.19%.
Walter White: Point-one-nine. There we go. So the whole thing adds up
  to... 99.888042%. We are 0.111958%. Shy.
Gretchen Schwartz: Supposedly that's everything.
Walter White: Yeah? I don't know, it just... it seems like something's
  missing, doesn't it? There's got to be more to a human being than
  that.
Gretchen Schwartz: What about the soul?
Walter White: The soul? There's nothing but chemistry here.

When I searched for it, Wikipedia has something different.
Which one is correct?

Not quite a dupe.

Neither are correct if you are looking for the "chemical" composition. Water, proteins, and fats are chemicals that make up most of the composition. Oxygen, hydrogen, carbon, and nitrogen are elements that make up those chemicals.

That conversation is strange. While different tables exist, the very first elements seem messed up. If the body is 60 (some sources say 70)% water, then oxygen has to be the most abundant element by weight (water - H2O - has a molecular weight of ~18 g/mol, with hydrogen contributing only 2g/mol of that weight).
The usual figures are roughly Oxygen (65%), Carbon (18%), Hydrogen (10%), Nitrogen: (3%), Calcium (1.5%), etc.
However, the writers of Breaking Bad weren't stupid. So, they weren't discussing percentages of the mass of each element, but rather the frequency of that atom in the body. The number of hydrogen atoms does indeed exceed the number of oxygen atoms.
So, by atomic percent, Oxygen is 25.6%, Carbon: 9.5%, Hydrogen: 63%, Nitrogen: 1.3%, Calcium: 0.24%, etc. So yes, the numbers are approximately correct for a normal, average, youthful (more water) 70 kg male.
So here is a table incorporating both percent by weight and percent by abundance. The writers were pretty well informed.


text:
What controls gut motility?
I have two different papers. One claims that gut motility is reduced by stimulation of the Opioid κ and δ receptors. The receptors are activated by Morphine and certain derivatives, specifically Codeine, Fentanyl, Hydromophone, Methadone, and Oxycodone.
The second paper claims that gut motility is reduced by blocking the 5-HTb3 receptors.  Antagonists or competitors to the 5-HTb3 receptors being Morphine and certain derivatives.
Are these two different theories, two different action mechanisms, or am I missing something?

They are two different mechanisms.

Opium is arguably one of the oldest herbal medicines, being used as analgesic, sedative and antidiarrheal drug for thousands of years. These effects mirror the actions of the endogenous opioid system and are mediated by the principal μ-, κ- and δ-opioid receptors. In the gut, met-enkephalin, leu-enkephalin, β-endorphin and dynorphin occur in both neurons and endocrine cells. When released, opioid peptides activate opioid receptors on the enteric circuitry controlling motility and secretion. As a result, inhibition of gastric emptying, increase in sphincter tone, induction of stationary motor patterns and blockade of peristalsis ensue. Opioid receptors in the gastrointestinal tract

Roles of 5-HT in health include control of normal gut motor activity, secretion, and sensation, and regulation of food intake and cell growth. Abnormalities of serotonergic function contribute to symptom genesis in functional bowel disorders, inflammatory and infectious diseases of the gut, emetic responses to varied stimuli, obesity, and dysregulation of cell growth. Therapies acting as agonists or antagonists of 5-HT receptors or that modulate 5-HT reuptake play prominent roles in managing these conditions... Serotonin and the GI tract.

Interesting. Gives me some more reading to do.  I assume at this time, the opioid receptors only work in one direction, to slow the gut.  Because not taking morphine does not cause diarrhea, but too much serotonin such as in carcinoid syndrome does cause diarrhea.

Don't rule out endorphins and their receptors in the GI tract.

What really burns me is that a treatment exists for IBS and depression that really works, Tianeptine (a serotonin re-uptake enhancer).  But is not legal in the US.  I have a trip planned next week to Nogales, Mexico.

When discussing the control of gut motility there is more to mention than the use of serotonergics and opioids - a number of peptide and nonpeptide neurotransmitters are important. Somatostatin and nitric oxide are two examples which each happen be inhibitory of intestinal motor function, but by two completely different mechanisms. A bit of understanding in cell biology, specifically cell signalling would be helpful to fully grasp this, but the former acts by inhibiting the release of Acetylcholine and Substance P while the latter increases levels of cAMP/cGMP. And don't forget about the basics when it comes to motor control - the cholinergics and adrenergics (including dopamine) are logical opposites.

References
Leung, P.S. 2014, The Gastrointestinal System: Gastrointestinal, Nutritional and Hepatobiliary Physiology, Springer, 19/03/2018, http://www.springer.com/cda/content/document/cda_downloaddocument/9789401787703-c2.pdf?SGWID=0-0-45-1491980-p176563984

This is a nice answer about gut motility, but the body of the question specifically asks about opioids and opiates, which you don't address at all. I don't mean to be condescending, but there's more to a question than just the title. I see you're new (Welcome!) Maybe you're not too familiar with the SE model? In any case, nice to have you here.

Hi, looking back at my answer I didn't really address serotonin either, thanks for the feedback. Can you tell me more about the SE model?


text:
Gastroenteritis virus causing mutation of the Enterochromaffin cells
I am working on the solution to a worldwide problem: IBS or chronic diarrhea following a viral gastroenteritis infection. I think I have an answer. The only missing piece to the puzzle I found in a research paper discussing the genetic mutation of the Enterochromaffin cells by a gastroenteritis virus. I believe the paper was from Japan.  I had it, but I lost it.  Any help in finding this paper again would be greatly appreciated.

Maybe this can be a jumping-off point?

Gastroenteritis virus + chromaffin + mutation gives no result on pubmed. I tried all combinations and variations. The closest is this article.


text:
Why are many anti-malaria drugs gap junction antagonists?
Why are many anti-malaria drugs gap junction antagonists?
My professor recently just mentioned that many of the anti-malaria drugs block gap junctions. i am wondering if this blocking is important for stopping malaria, and how blocking gap junctions is anti-malarial. How does this effect connect to the mechanism of malaria?

Could you give specific examples of antimalarials that block gap junctions? If they do, I'm pretty sure that this isn't anything to do with their antimalarial action. Most of the standard drugs interfere with the food vacuole of Plasmodium resulting in haem toxicity.

I wasn't sure when I first read this, but this is actually a very interesting question.
Right now there seem to be two completely divorced lines of inquiry that researchers are pursuing with respect to the antimalarial drugs.
One group of researchers is working on working out the mechanism by which say, chloroquine and its ilk bind to and  interfere with the formation of hemazoin (a parasite-friendly form of red blood cell proteins) in the vacuoles of the plasmodium (the parasite that causes malaria). Some folks have recently gotten some pretty reasonable crystals of chloroquine interacting directly with hemazoin. This all provides strong evidence for the view that, as regards killing plasmodium, the most significant interaction for an antimalarial is the one between it and hemazoin.
In (probably) unrelated news it was discovered that many of these antimalarials are also potent channel blockers of various kinds. I haven't dug into this too deeply yet, but most antimalarial people seem to view the channel blocking activity as a side effect. There are a number of other studies underway right now evaluating the psychological effect of the channel blocking activity of the antimalarials. There's one out of Iran that says that the blocking activity of Mefloquine can be used to ease the symptoms of morphine withdrawal.
Another thing to keep in mind is that Mefloquine fell out of favor not due to a decrease in efficacy, but was instead mostly taken out of circulation due to it's (justified) reputation for causing psychotic episodes in patients. So maybe this gap junction blocking stuff could be used to explain Mefloquine psychological side-effects. That would be neat!


text:
A subtle test for color-blindness
Is there a test method of proving a person being color-blind, without letting the test subject know, that he/she is being tested?
E.g. showing the person cards with colored dots like depicted here is not a valid answer.

How do you want to do this without test charts? You can only observe the person how it reacts on certain colors. If you can't ask directly, this will be hard.

i'm sure you could think of something, but the standard tests require asking questions.  just make a sign with two colors that would not be distinguishable and ask them to read it.

Once my chemistry teacher , who is colour-blind,  said...that the doctor during a standard eye test, told him nothing about colour-blindness, but showed him a chart, on which it was written- " I am not a colour-blind"....then when he was asked whether anything was written on the chart, he confidently & obviously unknowingly said "No"...

To what purpose does the nature of the test needs to be obscured?

Build a tiled floor with red and green tiles, write a really bad word with the tiles. Look for people who don't respond, then filter out the non-blind individuals who are too jaded to care.

Maybe the cognitive sciences SE may be a better platform for this question?

@Chris Stronks Thanks for the hint, I've also tried there.

Do consider ethics as well when hiding your true motives for subjects

@Chris Stronks Well, if it is ethical not exposing a person being color-blind in front of his/her peers, then I consider it ethical as long the results are kept undisclosed and unabused.

This question appears to be off-topic because it has been posted to CogSci.

I am colorblind, but I did not know that before I was 22 (!!). I got to know it by doing the Ishihara test. There are other tests you can do to test for colorblindness, such as the reverse colorblindness test (http://www.cs.unm.edu/~aaron/creative/colorTest.htm), where a "normal vision" person will not see the two patterns shown there.
Anyway, there is no test where you cannot ask "what do you see?" to the subject. On the other hand, I saw a photo where they were showing a northern light in both colorblind and normal vision (https://www.facebook.com/nlblog/photos/pb.236481989828593.-2207520000.1415264974./416457851831005/?type=1&theater) -I hope facebook links are OK in this site-, where I see no difference between the two photos. You could for example show that photo pair to your test subject and ask a set of questions (e.g. which one do you like more?). If he/she is colorblind, then the answer will be "they are the same", so you have a strong indication, or if they are able to point out differences, then they most likely have normal vision.
I could think of an experiment where you just show several photos with different contrasts/saturations, and then add the northern light photo (maybe the author has some other photos you could use), so they are not aware of the underlying question.
I hope this helps

I appreciate your hints (can't vote up, my rep is not high enough on this site). Actually I'm looking some method that is already scientifically proven.


text:
Why can't intermediate filaments be used as tracks by motor proteins?
A motor protein like kinesin-1 cannot use an IF as a track because it lacks polarity.
Can someone elaborate on this answer?

Just a guess: the IF doesn't have directionality. It would be like a single-lane, but two-way road.

Polarity essentially means a plus end (growing/polymerising) and a minus end (depolymerising). Look at microtubule (MT) (http://en.wikipedia.org/wiki/Microtubule). So molecules such as Kinesin-1 (http://en.wikipedia.org/wiki/Kinesin) use the hetero-dimeric nature of MT (alpha and beta subunits) and its polarity to orient themselves and move directionally along MT in an energy dependent manner.


text:
How do ants know where they are going without eyes?
I know that ants have some sense of direction, but what is the physiology behind this sense?

The eyes are easily seen on green ants. In other genera you may have to look more carefully to notice the eyes.

Well, first off, they have eyes, so there's that.
However, a lot of what ants wish to achieve can be done through a combination of a random walk and chemical trails.
When ants are exploring their surroundings, they are essentially wandering about without much in terms of a sense of purpose; laying down a chemical signature as they go.
When they find something interesting, like food, they use their own chemical trail to backtrack, laying down a new chemical trail indicating the nature of what they have discovered, making a kind of smell-road from the hill to the point of interest.
Any ants that subsequently come across this trail follow it, and subsequently join in transporting the food back to the hill.
An interesting implication of this behaviour is the antmill, wherein an ant will lose their trail, and revert to following a nearby ant. If the ant they follow are following them to begin with, this can lead to a spiral of ants that can reach miles in diameter, consisting of confused ants walking until they die from exhaustion.

This is the correct answer. The behaviour just described by Williham is btw so simple (though effective) that it can be modelled in simple agent-based simulations. The underlying set of rules is a very basic one. One example: https://www.youtube.com/watch?v=UZ2HTTeM3aQ

Kindly elaborate more on the "chemical  signature" part? @Williham Totland

@Cupidrex That was just me being unclear; I meant chemical trail as in the other paragraphs; and strictly speaking antmills arise due to ants following one another by sight, not smell.


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What Aquatic Mammal has no Tail?
Found in a waterway in Butte County, CA. First thought it was a beaver kit, but it has no
tail.
What aquatic mammal has no tail?

Are you sure there is no tail? Muskrat?

Muskrats have a rat tail. This critter may have had a small knob of a tail, but the hair at the hindquarters was too wet to reveal much of anything.

Your individual might have had an accident in the past!

What size is it? I'd agree with kmm and Remi.b that it's a muskrat which lost its tail.

What a great picture!

Looks like a mountain beaver (Aplodontia rufa) to me. Location, appearance, and minimal tail all match.

A bit more detail:
Where I'm from on Washington's Olympic Peninsula, they're not uncommon, but Butte County is near the southern end of their distribution (eol map page) and they may be less common there, and limited to cooler higher elevations (Beier 1989), and to wet habitats (their inability to concentrate urine (!) means they need to drink enormous quantities of water).
This white paper from USDA (Arjo 2007) is a great source, and more comprehensive than the  the wikipedia page, which is also good.

Arjo, Wendy M. (2007). "Mountain Beaver: A Primitive Fossorial Rodent". USDA National Wildlife Research Center - Staff Publications. Paper 675.
Beir, Paul (1989). Journal of Wildlife Management 53(3) 649-654

Hey, Oreotrephes, thanks for taking the time to respond with the correct answer.
This is a video I shot of this animal, and it reveals that it definitely is the mountain beaver:
http://youtu.be/8Ljp1NiLvLU

Aw, what a cute little guy. Great footage!


text:
Regarding apoptosis and inhibitors
If there is an apoptosis shut-off mechanism of any kind, one could call it a null-apoptosis mechanism.
If this is possible, could there be a null-apoptosis inhibitor? Something that inhibits an apoptosis inhibitor?

Apoptosis is very tightly controlled for obvious reasons. Setting it off without proper control would result in the uncontrolled loss of cells. Apoptosis is one of the major pathways which are either mutated or shut-off in cancers, preventing the body from eliminating malingnant cells. These two papers are interesting in this context:

Apoptosis: A Review of Programmed Cell Death
The role of apoptosis in cancer development and treatment response

In this context it makes no sense to have a shut-off mechanism once the apoptosis cascade has started. It is only set off when there is a real reason (and is well controlled), so I don't think there a "null-apoptosis" mechanism. It would of course still be possible to artificially make substances, that inhibit parts of the activation cascade. But besides for apoptosis research I don't see any use for it. There is actually some research going on to find out how to activate apoptosis again in cancers.

What about 'something' that could inhibit some pathways or mechanism that is about to shut down or turn off the apoptosis mechanisms? An Apoptosis Inhibitor Inhibitor ( if you could call it that)..

There are mutations or dysregulation occuring in cancer which actively shut down apoptosis. You could of course think about designing molecules which could do the same. But to my knowledge they are not occurring naturally.

Could DNA-polymerase or something like this correct any genetic mutations or genetic 'mis-configurations' in a cell that may be causing the apoptosis mechanisms to be shut off?

I don't think the DNA polymerase could do that, as this enzyme is only directed to promoters which are active. When apoptosis is shut of due to epigenitic silencing or mutations, that is usually not reversible by the cell. There is research being done if this can be reversed in cancer cells to promote apoptosis there and get rid of the cells.

If a cell has had its apoptosis mechanism shut down and it then reproduces or is 'forced' to reproduce would its daughter cells develop in a way where their apoptosis mechanisms malfunction? If this is so would this develop a cancerous group of cells?

This is exactly what happens in cancer. To be able to grow and metastasize the tumor needs to overcome apoptosis. Have a look at this and this article.


text:
Can cancer cells in the same person, organ, and origin have different DNA?
Is it possible for cells from the same tumor to have different genetic material, and if so, to what degree is it possible (how fast do they mutate) ?

Cancer cells and normal cells differ on the genetic basis but they share the same genetic background, so they have not different DNA in the sense of two different people. They have to be different, since cancer cells have to accumulate mutations on a number of genes to become a cancer cell, which can survive and will not be directed into apoptosis. These are genes which control the cell cycle, certain growth factors, tumor suppressor genes, cell signalling and so on. In all these genes there need to be either activating or deactivating mutations present. Most of these mutations are point mutations (single nucleotide polymorphisms, SNP), where only one base is altered to achieve a mutation. An example for such a mutation would be the mutation in the B-RAF kinase, which is involved in signaling and activating genes, where a point mutation exchanges Valine 600 to glutamic acid (V600E, for reference see here). These are relatively small differences between these two cells. The Cancer Genome Project aims to sequence cells from a cancer and also normal cells from the same individual and then do a comparison. Later stages tumors often tend to genetic instabilities where complete regions of the genome are duplicated, inverted or deleted, see here for a review.
A more basic overview is given by the Ebook "Essentials of Cell Biology" by the Nature Group, which has an overview of cancer cells.
Regarding the mutation rate, this is hard to estimate. There are a few papers available here, but they focus on the mutation rate in germ cells, so these are mutations that are transmitted to the next generation. The estimates there are between 70 and 100 mutations per generation per individual, depending on the research method. You can find a nicely explained blog article here, which gives a number of original references, too.
The mutation rate in cancer is a different thing, since this depends on which genes are mutated. The mutation rate for cancer has to be higher for the cancer cells to allow to collect the necessary transformations into a cancer cell, but these mutations seem to occur only in a few hotspot regions of the genome (Further references can be found in this article called "The causes and consequences of genetic heterogeneity in cancer evolution" and in this called "Emerging patterns of somatic mutations in cancer"). There are two article called "The mutation rate and cancer" which are interesting in this context. They can be found here and here. As always, if you have problems with getting the articles, let me know, I can help there.

Your answer is good but if I am not mistaken, the OP is asking "Is it possible that two cancer cells (which originate from the same cancer) to have different genetic material?" And more interestingly, "What is the mutation rate of the cancer cells? Is it alike other cells, lower or higher?" Could you develop your answer?

I worked on it now that I could reach the Pubmed again.

@ Chris & @Remi.b excellent "what I need exactly ", thank you very much.

A) It absolutely is very common for extensive genetic heterogeneity to exist in tumours, including between individual cells. Talha already posted links to some very good reviews from Charlie Swanton and colleagues so I will just add in a citation for single cell evidence here ( http://www.nature.com/onc/journal/v36/n20/full/onc2016438a.html )
B) As for mutation rates - they tend to markedly vary across cancers and across regions of the genome based on replication timing and chromatin boundaries. Given the variation in the total number of mutations accumulated and assuming that a similar number of cell divisions , given birth and death rates, are required to get to a typical clinically observable tumour there must be variation in the underlying mutation rate.
Such variability may have much to do not only with background rates of mutagenesis but also with deficient repair mechanisms coupled to it, and there are clear examples of aberrant repair contributing markedly to mutational burden, including mismatch repair ( http://www.nature.com/onc/journal/v36/n20/full/onc2016438a.html ) and homologous repair defects ( https://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3934.html ) and mutational processes (UV-induced and smoking induced cancers have particularly high mutational burdens)
http://www.nature.com/ng/journal/v46/n8/fig_tab/ng.3006_SF1.html


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Queller's 1985 version of Hamilton's rule
Queller 1985 ("Kinship, reciprocity and synergism in the evolution of social behavior") provides a generalization of Hamilton's rule that allows for non-additivity. To accomplish that, Queller writes the fitness of an individual as
\begin{align}
  W = W_{0} - CP + BP' + DPP'
\end{align}
where $W_0$ is the baseline fitness; $P$ is the phenotypic value (1 for altruist or 0 for nonaltruist); $P'$ is the phenotypic value of the interacting individual; $C$ is fitness cost if $P=1$; $B$ is the fitness
benefit if $P'=1$; $D$ is the deviation from additivity of $C$ and $B$ if
both were altruistic (i.e., $PP' = 1$).
Queller then substitutes this equation into Price's equation $\Delta G = Cov (G, W)$, where $G$ is the frequency of altruism allele in the focal individual($0$, $1/2$ or $1$). The resulting equation is:
\begin{equation}
  - \bar c + \bar b \frac{Cov(G,P')}{Cov(G,P)} + \bar d \frac{ Cov(G,PP') }{Cov(G,P)} > 0
\end{equation}
where $\bar c$, $\bar b$, and $\bar d$ are the sample means of $C$, $B$, and $D$.
My question is: how did Queller arrive at the sample means $\bar c$, $\bar b$, and $\bar d$? I understand that $Cov(aX,Y) = a\, Cov(X,Y)$, provided that $a$ is a constant. But what Queller is doing here is different; he seems to be saying that $Cov(AX,Y) = E(A)\, Cov(X,Y)$.

It is just worded a little wierdly in my opinion. The key line in the paper is: 'Fitness components are also defined for all individuals, for example, $C$ is defined, even for a non-altruist, as the cost it would incur if were altruistic.'
Essentially, if it doesn't matter what individual you are you always pay the same cost, then $C$ is a constant. This is pretty much the definition of a constant! The expectation of a constant is just the constant, $E(C) = C$.
The reason it works is that to find whether or not the cost is realised, Queller simply multiplies by the focal individual's phenotype value $P$, which is either 0 or 1. So either the individual pays the cost or it doesn't.

I think Queller's discussion of his 1985 model in his 1992 paper "Quantitative Genetics, Inclusive Fitness, and Group Selection" (p. 552) is better worded. There he writes the C, B, and D as regression coefficients.


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Identifying whether ELISA kits are authentic or fake
What methods can be used to determine whether they are authentic or fake?

You are getting this Elisa Kit spam from China, too? The only way I see, would be to use a known reference standard so you can titrate both the specificity and the sensitivity of the kit. Ideally you would compare it with a known and proven kit. If you have the reference available in the lab and the cheap kit is not too expensive you can give it a try. I would do it, since work time and reagents also cost money.

the problem is, one of the reasons these kits are so expensive (at least the ones from reputable companies) is because they spend time and money to make sure the kits actually work and give reproducible results. For me, if I don't trust the quality of the supplier, why would I even think of possibly compromising the integrity of my data with substandard reagents?

Its the same for me. I don't order from suppliers where I am not sure about the quality. We routinely test substances from cheaper companies but there we either get tipped by colleagues or the stuff is so much cheaper, that we can give it a try. I don't see this for Elisa kits. And even if one batch is ok it doesn't necessarily mean that the next is as well. From the known suppliers we can be sure.

Just a few direct ways can figure out whether Elisa Kits are authentic or not.

Proposing to visit their factory. Generally bait company does not agree with it.
Complete range of kits. If a company has every and each ELISA Kit, it is usually fake. Unless they are very large  and professional companies, such as abcam, cellsignal, sigma, sabbiotech and so on.
See the price. If prices are ridiculously low, but in the name of large companies such as import R&D raw materials packaging. This ridiculously low price can't even afford the raw materials, which company will sell at a loss?

This problem is rampant and has been plaguing the research community for a decade. I can explain how exactly do these companies make these fake kits, how to experimentally verify what I said is true, and how to spot them by just looking at their website. I can even point fingers and name a few known and notorious companies that do this malpractice. What I ask from anyone who reads this is to recognize that these companies are the bad apples in Chinese companies and you shall not generalize all Chinese biotech companies. Generalization, not a good thing, and I trust all the years of training in scientific critical thinking has taught you better :)
Now how do these companies make fake ELISA kits? Simple. They use a universally present protein target, initially TGF beta--I do not know what they have shifted to lately--to make one type of ELISA kit, and label it as anything and everything.
How to actually prove it? Run a western using a trusted third party antibody. If nothing shows up, you know the standard is not what they claim it is. Or you can also run a third party recombinant protein on the kit. Same core concept.
Do not want to bother with all that? Then just keep an eye out for this signature: one company that has thousands sometimes tens of thousands of ELISA kits, covering all kinds of species--sometimes ridiculous ones like whales, giraffes, tadpoles, sharks etc.--nothing against giraffes, they are awesome and all but seriously... These companies are literally like Noah's Ark. How can one company you never heard of come up with so many ELISA kits while established companies who have been making kits for decades are dangling on the level of hundreds or thousands?
Maybe, one thinks, that someone went hard core and just made them all, that maybe this is real? After all there are no other choices, they are the only ones selling this ELISA kit, wouldn't hurt too much to give it a try...??
And that is why these companies still exist today. That is why so many papers got pulled, and so many clinically promising indications turned out to be false. That is what cost millions of dollars of tax payers money.
At the end I want to point out that, if researchers did their due diligence, or if there are some more effective forms of media where researchers can get information like this, these companies would have died a decade ago. Instead they just keep coming up with different company names and pulling the same scam.
I want to put examples of these companies by directly referencing their names but I am not sure about the forum rules would allow it so for this post, I would not do so. The signature described above should be clear enough for you to spot these companies. Wish you all the luck in 2015.


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Is an antivenom venomous?
What happens when someone takes an anti-venom for an animal they weren't bit by, either for incorrect identification of the animal they were bit by or if they weren't bit at all?
I am looking for the immune system reaction, and possibly why it reacts as it does.

@jonsca Why the edit to change antivenom to antivenin? From Wikipedia: "The name "antivenin" comes from the French word venin, meaning venom, which in turn was derived from Latin venenum, meaning poison.
Historically, the term antivenin was predominant around the world, its first published use being in 1895.[2] In 1981, the World Health Organization decided that the preferred terminology in the English language would be venom and antivenom rather than venin and antivenin or venen and antivenin."

@AlanBoyd Feel free to roll back.  I was always taught that "antivenom" was incorrect.

It seems like there's a mixture of both in the literature, and Webster's defines "Antivenom" as "Antivenin".  I will leave it be, though.

@jonsca I searched for both words as title terms at Web of Science: antivenin has total hits 190, 104 (54.7%) since 1981 whereas antivenom has total hits 598, 561 (93.8%) since 1981. It looks like the WHO decision was pretty influential. Incidentally I have no axe to grind on this, I was just curious since I don't recall ever seeing the word antivenin before your edit.

@AlanBoyd I guess who can really argue with the WHO, then?  I have enjoyed learning more about the usage of the word, so thanks for enlightening me.

usually the antivenoms are antibodies raised against these protein based venoms. Serum injections may cause anaphylactic reactions but should otherwise be safe.

https://books.google.com/ngrams/interactive_chart?content=antivenom%2Cantivenin%2C+ANTI-VENOM&year_start=1800&year_end=2000&corpus=15&smoothing=3&share=&direct_url=t1%3B%2Cantivenom%3B%2Cc0%3B.t1%3B%2Cantivenin%3B%2Cc0 @AlanBoyd

Although it is fancy to think of antivenom as a poison for the poison, technically it is a poison only for the poison!
Antivenom is developed in horses (equine) by hyperimmunizing them against the particular venom at a non-lethal dose, followed by collecting the serum. Venoms are complex and have many enzymes and hence are proteins. So, antivenoms are just antibodies against the venom proteins.
Moreover, the antivenoms are classified into monovalent and polyvalent. This signifies whether the sera was prepared by hyperimmunizing the animal with the venom of a single species or many common venomous snake species together.
Usually, a snake bite is an emergency and the victim or the attendants rarely identify the snakes (In our place, patients sometimes to our surprise, even bring the killed snake to the casualty!). Hence, to avoid confusion polyvalent sera are used.
I've written all this just to make an impression that polyvalent sera also carry antibodies against the wrong snake too, but at the end of the day, it's the right antibody that does the job.
As mentioned in the comments, apart from occasional anaphylactic reactions or serum sickness, they are pretty safe (cost/benefit) to use.


text:
Western blotting of lung samples
I have been working on lung samples to perform western blotting. I have two related questions about this:

I get very nonspecific results: at times nothing at all, at times it glows on membrane but doesn't take up on x-ray film. What are the common causes of these errors and how might I avoid them?
I am interested in assaying GPCR expression. When I am assaying for GPCRs, do I need to prepare the lung samples in a specific way (that is different from sample preparation for Western blots of other proteins)?

You may be interested in this: http://biology.stackexchange.com/questions/7205/how-to-do-western-analysis-to-lung-tissue

I wrote the answer to the above question, please let me know if you're still having issues. Just leave a comment with @MattDMo in it.


text:
How does fever physically work?
What is the physical mechanism that causes temperature to rise during a fever? I know that somehow the hypothalamus "orders" to increase the standard body temperature regulation, and this should stimulate mitochondria to produce more ATP. Is that right?
Is this the only heating physical mechanism (through increasing production of ATP) that acts during a fever?

From Wikipedia: "The [hypothalamus] ultimately orchestrates heat effector mechanisms via the autonomic nervous system. These may be: (1) Increased heat production by increased muscle tone, shivering and hormones like epinephrine; (2) Prevention of heat loss, such as vasoconstriction.
In infants, the autonomic nervous system may also activate brown adipose tissue to produce heat (non-exercise-associated thermogenesis, also known as non-shivering thermogenesis). Increased heart rate and vasoconstriction contribute to increased blood pressure in fever."

As John mentioned, pyrokines such as IL1 and TNF affect the hypothalamus. Your hypothalamus is a thermostat, similar to central heating for example. So when you set your core temperature higher, your body thinks it is cold. To warm up it does several things:

Vasoconstriction directs blood to the core body and prevents heat
loss
Brown fat break down in infants makes heat
Shivering which requires respiration which produces a lot of heat. Metabolism also
increases in other ways - this is why it is commonly advised to
increase food consumption during illness
We wrap up warm - an often overlooked mechanism that is incredibly important.
Limited piloerection: if we are hairy our hair will stand up attempting to
create a barrier for heat loss
We stop sweating (breaking of a fever or when the hypothalamus is reset to normal causes us to sweat)
Hormonal regulation via (nor)adrenaline/epinephrine, thyroxine - these are related to the increased metabolism.

Cytokine production in the body resets the thermoregulatory centre in the hypothalamus to a higher temperature. As a result, your muscles begin to contract violently (rigors) to generate more heat until you equilibrate to the new setpoint. Hope this helps.

Yes but just to mention the reset is to a higher temperature. From 37 to 38 for example.

@AndroidPenguin Thanks for pointing that out-its a higher temperature. I'll edit my answer.


text:
$S_{0.5}$ vs $K_m$ values in enzyme kinetics
What is the difference between $S_{0.5}$ values and $K_m$ values in enzyme kinetics?

What do you mean by S0.5? $K_M$ is the concentration of substrate at the point when the rate of the reaction is 0.5 of the maximal rate ($V_{max}$).

I edited the Mathjax into the title as well, as it seems to yield an appropriate URL slug: http://biology.stackexchange.com/questions/5004/s-0-5-vs-k-m-values-in-enzyme-kinetics

Km applies to a data set exhibiting MM kinetics, i.e. it has a "mathematical" underpinning. Presumably S0.5 is simply the observed substrate concentration for 0.5 x Vmax regardless of whether the data fit MM?

probably worth looking at http://biology.stackexchange.com/questions/3147/is-the-ec50-of-an-activating-protein-for-an-enzyme-a-good-indicator-for-the-bind

This expands my comment on the question to an answer.
If an enzyme exhibits Michaelis-Menten kinetics, then it is valid to define a KM and this equates to the substrate concentration when reaction velocity is 0.5 * Vmax.
However, many enzymes do not exhibit Michaelis-Menten kinetics. One example is when the enzyme shows a co-operative response to substrate concentration. In these circumstances the substrate concentration when reaction velocity is 0.5 * Vmax is still a useful parameter, but there is no KM.
See this paper for a discussion of the kinetic properties of the glucokinase of pancreatic β cells, which acts as the glucose sensor. This enzyme shows positive co-operativity with respect to its substrate glucose, and the authors develop a kinetic analysis in terms of various parameters. These include an S0.5 value for glucose, but a KM value for ATP (presumably because the kinetics with respect to ATP are simple Michaelis-Menten).


text:
Are there any websites offering graphs for the light absorption of different enzymes?
I have found graphs for the light absorption of water, haemoglobin, lipids, melanin, etc., but I am having a hard time finding graphs about enzymes.
Are there any websites or other reference sources for this type of information?


text:
What data / tools exist for mapping of disease trends?
I was just looking at the Google Flu Trends map.  Google Insight could be used to gain similar information for other trends in disease keyword searches.
I started wondering how valid are keyword searches to represent the spread of diseases.  In some ways I think it could be a good representative, but in others I think it would be susceptible to influence by mass media.
Do maps of clinical data exist that could be compared to this Google data?  If so, where could I find some.  =)

You can use official sources such as hospital admissions, prescriptions for drugs fighting the disease you are tracking, sales of over-the-counter medicines.
CDC (cdc.gov/flu/weekly/, cdc.gov/outbreaknet/outbreaks.html, etc), WHO, EuroFlu Weekly Electronic Bulletin map official clinical data, Aurametrix uses these sources.
Several scientific studies have compared GFT, twitter, even facebook with official sources.  Johns Hopkins study (pubmed/22230244) used data from local hospitals in addition to CDC.
My sampling studies too showed that social trends are surprisingly good, despite all the noise, but provide good estimates only for highly populated areas.
You might also want to check Sickweather's algorithm, healthmap, usgs disease maps and industry databases providing coverage of pharmaceutical companies and product sales.

For myself, I've not been terribly impressed with the use of keyword searches and the like as methods of predicting influenza or other diseases. They are, when it comes down to it, somewhat glorified extensions of a syndromic surveillance system, just for "I feel sick" instead of "Honey, pop down to CVS and pick up some NyQuil?"
It's also apt to get you some odd results. I tried to use a "Google-style" analysis to match some rotavirus data to Google searches - I believe I was 7 entries down before I ever got to anything rotavirus related, and even that was "rotavirus", which doesn't suggest it would be useful as a symptom detector, but rather people Googling a disease their doctor said they had. The top results, some of which fit really well? A series of prom dress-related searches. In order for it to be useful, you'd have to extend Google's system.
But, as a thought experiment, if you'd like to match it to data, there's a number of potential data sources publicly available from the CDC. Morbidity and Mortality Weekly Report for example publishes weekly counts for a number of notifiable diseases.


text:
A timeline of the odds for survival for fertilized eggs and fetuses
I'm looking for data to build a timeline of the odds for survival of a fertilized egg, i.e.,

What are the odds it'll last a week?
What are the odds it'll last a month?
2 months?
(and so on until)
What are the odds of it being born?

I am interested in the odds with the usual level of care in an industrialized nation (and a mother that is not trying to abort the fetus).

Not exactly what you are looking for, but kind of related: http://4dpiecharts.com/2012/06/15/how-long-does-it-take-to-get-pregnant/

here I found an answer. Not sure how accurate is is, though.
Data seems to be from the US
Here is a rewrite of parts of that article:

266 days before birth, all we have is a fertilized egg.  (~33% chance of living birth).
The odds are calculated using data from in-vitro fertilization, and the next stage is 66%.
In in-vitro, some 50% of the eggs cannot fix to the uterine wall
262 days before birth, the egg has implanted (~66% chance of living birth)
After implantation, there is still a decent chance that the embryo will be aborted (and maybe the woman will not even know that she was pregnant).
Half of the embryos that die from here on will die because of chromosome abnormalities.
241 days before birth (~88%)
178 days before birth, entering the second trimester (~97%)
At this stage, problems are more likely to stem from the mother, not the fetus' genome. Problems with the cervix, the uterus or the placenta are (some ?) likely causes of death.
89 days before birth, entering the third trimester (~99%)
At this stage, doctors will consider the fetus a patient, and treat it if needed.

Maybe you could summarize a little bit the content of that page, in case it went down in the future.


text:
How to give a biological interpretation to this phase portrait?

Consider the following system and analyze its behavior.
$$\begin{array}{rl} \frac{dA}{dt} &= A \left( 2-\frac{A}{5000}-\frac{L}{100} \right)\\ \frac{dL}{dt} &= L \left(-\frac{1}{2}+\frac{A}{10000} \right)\end{array}$$

The analysis
It has $3$ equilibrium points. I know the stability of the three points but I am not sure if I interpret the meaning of them correctly according to the phase portrait. $x_1, x_2$ are saddle points and $x_3$ is stable point they are
$$\overline x_1=(0,0)$$
$$\overline x_2=(10000,0)$$
$$\overline x=(5000,100)$$
According to the phase portrait I think the behavior of the system is described as:
For every point $(A,L)$ given in the first quadrant, where $A$ is the number of aphids at time $t$ and $L$ is the number of lady-bugs at time $t$, we'll have that in the future, the maximum number of lady-bugs and aphids it's going to be $(5000,100)$ respectively. This also means that both population will never going to extinct.
Even in the case where there were just a few number (near 0) of lady-bugs, their population will grow and will be establish also.
My question
Did I miss something important in the biological description to the phase portrait?

You seem to once put bars over your equilibrum conditions and once not. I am not sure they are exactly the same. Also, I think you once meant $\bar x_3$ instead $\bar x$. Note that the usual is to use a hat rather than a bar for an equlibrium.

I don't think you missed anything important!
You could investigate the cyclic behaviour around the equilibrium. For example, looking at the variable aphid population size can start above its equilibrium point, then overshoot it and overshoot it again to finally reach the equilibrium point. If you zoom close to the equilibrium point, you might see long cyclic behaviour before ever reaching the equilibrium.
You sure could do all kind of further analyses such as a stability analysis or searching for cyclical equilibrium but it is easy to see with this simple model that nothing very complicated will arise. You could also investigate for what parameter values this classic pattern breaks up if it does.
Another option is to make the model more complex by introducing a carrying capacity (and then investigate under what aphid growth rate the behaviour becomes chaotic), or population structure, or whatever.
You might learn much from it but you might still want to have a look at the post What prevents predator overpopulation?.
I highly recommend the book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto and Troy. It will show the typical kind of analyses that can be done for this kind of systems.

I don't see a cyclic behaviour. Cyclic means something circular ?

If you start at (15000, 300), you'll circle around the equilibrium. Maybe not a full circle though. I don't know. But both variables are going to overshoot the equilibrium at least twice.

You're right, haven't notice. Also you mention that I could make the model more complex by introducing a carrying capacity. Exactly how would be that term? I mean something like +1/k or -1/k

@Anneliset. Remember, when you are modeling biological data like this you are plotting means, but in the real world you are going to have some added noise. That means that even if you have a stable fixed point like in this phase diagram, if you actually simulate data rather than means you are going to oscillate a bit around it because a noise term keeps you in the 'cycle' and prevents settling to perfect stability.

Carrying capacity would typically like like an added $\frac{K-N}{K}$ term that multiply the rest. See logistic population growth. It is quite classic. You might want to read an intro book on the subject rather than having to reinvent the wheel by yourself. You might want to have a look at a population biology books. I had one in mind which is apparently very good but I can't remember the title or author right now.

You can ask for book recommendation on another post if you want. Here is a book recommendation post for population genetics.

I was wondering, time $t$ is measured in what units? days or months?

Typically measured in generation time. Your model must assume equal generation time (and non-overlapping generations) or must consider that the values are adjusted for differential generation time.

Oh ok, I was observing the model again and I've seen that there exist competence between aphids due this term $-\frac{A^2}{5000}$, why aphids compete in nature?

Sure.... there is always competition among individuals in pretty much any species.

But you are a biologist , you must know why they compete.Is it for food or ...? (I won't bother again, this is my last question:) So if you don't mind, answer me.

Well... I am not an aphid biologist! I am a theoretician (mainly numerical stuff, not much analytical) in population genetics. Also, it is the kind of question that would deserve its own post. I don't know the answer and I typically don't seek much in the literature for a follow-up question. I (or other users) might do it on another post. There is probably competition over habitat (incl. for leave where they make their galls), food, protection from ants, etc...

You can just go on Google Scholar > Aphid competition and you'll find some answers. Good luck @Annelise!

@Remi.b The model already has a logistic/carrying capacity component; the second term of the aphid equation can be rewritten as $-A^2/5000$, which could be interpreted as a carrying capacity of 5000 (or that $r/K = 1/5000$).


text:
What makes a wet dog so stinky?
Similarly, what makes a wet down comforter so stinky? Why do they make no smell except when liquid is added?

I don't think pheromones play into this at all.

I would say this would have to do with the proliferation of fungi...

This is kind of a physical chemistry question really as it is related to the evaporation of volatile compounds rather than biochemistry specifically.

Thanks for the tag change. It wouldn't let me create tags and dog, fur and feathers didn't exist. (Probably good that it didn't let me create tags...)

From this source,

We answered this question on the show...
We posed this question to Dr David williams from the Veterinary School
  at the University of Cambridge... David -  First of all, what actually
  makes something smell?   Molecules have to leave the smelly objects
  and get to your nose through the air and that means that these
  molecules must be very small and volatile.  That's to say they must be
  easily evaporated.  The chemicals that make dogs smell are mostly what
  we call volatile organic acids and they are produced by bacteria from
  the fats that are breaking down from sweat; and that's maybe why we
  find these body odours unpleasant.  They signal a presence of bacteria
  and decay and death to us.
Their [dogs] skins mostly have
  Staphylococcal bacteria, which don't produce much in the way of a
  smell at all, but they've also got some yeasts too which are really
  pongy.   But why does the smell seem worse when the dog is wet?  Here,
  I think we have to go into some physics.  The amount of evaporation of
  a substance is related to the concentration of the compound on a
  surface it’s evaporating from and the amount of compound that's in the
  air, just above the surface.
So how might that change when it’s wet?
Well, if the organic acids are dissolved in water on the fur of the
  wet dog, as the water evaporates, the concentration of those smelly
  acids increases, so they'll evaporate more, so there are more
  molecules in the air for us to smell.  Diana -   A bit of evaporation
  can effectively amplify the amount of volatile chemicals that emanate
  from a dog’s skin, and Dr. Williams thinks it’s the same effect that
  causes that damp earth smell when it rains.  It may also alter how
  dogs interact with each other when they're wet.  So, if you have a
  dog, watch to see if it sniffs differently at other dogs on a dry day
  versus a wet one...

There's a start, sounds legitimate to me...

Excellent! And I had read somewhere that "after rain" smell is due to rain drops pummeling the ground and dusting up molds. This makes much more sense to me. Thanks!

The "after rain" smell is technically called "petrichor". In summary, compounds from plants emitted during dry periods get absorbed into rocks. Rain releases these compounds and the smell derives from these compounds. The wikipedia page is a good place to read more about petrichor.

And that's why flatulence smells more in the shower.


text:
When did vision evolve for the first time?
Today I wondered what the first organism to evolve vision would have been. I assume that it would have been kind of primitive and basic, but of course extremely innovative and eventually useful to a wide variety of beings.
It also makes sense that the evolution of vision would have accompanied the evolution of advanced brain functions in almost every case. So, do biologists have any idea as to what the first species to use vision would have been?
(By vision, I mean having some organ on your body that receives photons and has some signaling pathway that converts photons into a biochemical set of signals)

I think I read in one of my textbooks that vision likely arose from  photoautotrophs developing a photosensitive spot in their cells.  This was advantageous as the organisms could move into areas where light conditions were favourable

What do you mean by vision? How complicated of a system? Photoreception has a long evolutionary/phylogenetic history and can render a fitness advantage without an eye or central processing unit. But as for eyes/brain, that's a different question, I think.

vision has evolved independently at least 10 times, likely more.  the simplest multicellular vision system we know of is literally one light sensitive cell attached to a single nerve cell. that nerve cell is inhibitory, it inhibits the swimming muscles impulse on that side of the worm, making the worm turn towards the light.

I'll address the question in the title "At which time did sight evolve for the first time?" by assuming that by the evolution of vision, we mean the evolution of the eye.
Molluscs are an excellent phylum to investigate this question because they exhibit a wide range of eye designs and levels of complexity.
At the most basic level, limpets such as Patella exhibit small patches of photoreceptor cells lying in a relatively flat configuration. Slightly more advanced is Pleurotomaria which has photoreceptors and pigmentation cells held in an eyecup. We then have the pinhole camera style eye as seen in Nautilus (see this post), and more complex eyes with a cornea, retina, and lense such as those seen in squid (e.g. Loligo).
Assuming that "a patch of photoreceptors" in an animal counts as an eye, then we should probably looking for marine invertebrates. The problem here is that if they had only soft body parts we might struggle to identify the oldest examples in sediments.
One candidate for the "earliest eye" might be urbilatarians - the hypothesized last common ancestor of the clade bilatarians - which probably evolved at the end of the Ediacaran period (~555 Myr). An example would be Kimberella (described here) which might or might not have been a mollusc and might or might not have had photoreceptors!

(credit : wikipedia)

"To me, it also makes sense that the evolution of sight would have accompanied the evolution of advanced brain functions in almost every case."

Not necessarily! For instance, think of phototropism: the plant detects the presence of light and uses it to grow towards the light, but that's a very simple process regulated by auxins. Or the light-sensitivity (phototaxis) shown by Euglena, a single-celled protist, which reorients its entire body towards a light source. Really simple vision (is there a light, and if so, where is it?) can help organisms absorb more energy than rivals, giving them an evolutionary advantage.

It also makes sense that the evolution of vision would have
  accompanied the evolution of advanced brain functions in almost every
  case.

Untrue. Behold the box jelly. With eyes that have similar structure to vertebrate eyes. Able to form an image but yet no brain to understand what it is seeing. http://www.livescience.com/13929-box-jellyfish-eyes-navigation-brain.html
Also a single cell organism (warnowiids) that may have an eye (retina and cornea like structure).
http://phenomena.nationalgeographic.com/2015/07/02/single-celled-creature-has-eye-made-of-domesticated-microbes/