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What are tail currents?

This is a voltage clamp on an ion channel. When the voltage is stopped there is a still a current at the end (the tail current). I understand that the gates aren't completely closed because of which there is still some current flowing.
What I don't understand is that why does the current suddenly jump to a small value? Shouldn't it gradually go down?

I'm voting to close this question as off-topic because  it appears to be a physics question

@rg255 it's Biophysics and on protein ion channel gating. Bio, most definitely

This trace looks a bit funny - I am guessing the OP has abandoned the site, but if OP happens to return and can give a source for this image that will really help with providing an explanation specific to this example.

@BryanKrause Fwiw, an image search yields no other copies of that image, however, figure 4 of this paper shows the same effect.

As for an answer I have no idea but in general electrical systems you would expect a sudden jump like that if a switch/gate was opened or the voltage was cut. Without knowing anything about this topic, from an electrical perspective that signal still seems to be reasonable to me (not that that means anything of course). As a wild guess I'd assume the slight curve after the jump is due to capacitance somewhere downstream of the gate? Or some complicated thing with the kinetics of the gate that I don't understand.

@JasonC I also attempted an image search with no success; I agree that Figure 4 of the link you share does show nice tail currents, but it doesn't show the rapid jumps in current that the OP's picture shows, and the "tail currents" there also look funny: they increase then decrease, rather than the smooth decay of normal tail currents like the article you link. My suspicion is that there is some artifact contributing in the OP's post.

@JasonC The artifact would be from a failure to normalize the pipette capacitance. So it wouldn't have anything to do with the biology but rather an incorrect setup of the patch clamp amplifier. In a good electrophysiology experiment you should not see that artifact, the traces should look like Figure 4 of the paper you linked.

@JasonC And to explain the biology a bit, there are two things going on here: 1) The experimenter is applying a constant voltage using a patch clamp amplifier. On each trial, that constant voltage starts at one value, briefly steps to another value, and then back to baseline. 2) The step in voltage is activating voltage-gated ion channels. The opening of these biological channels changes the amount of current that needs to be applied to maintain the voltage specified - that current reading is what is plotted in the OP's figure. Those channels do not close instantly, which produces tail current

OK, I know this is old, but here goes. The tail current is the current at -55mV after the voltage step, here:

The current shrinks as the voltage changes, this causes a massive shift in the driving force for the ions either side of the cell membrane. Going from -125 to -55 mV for the largest step. As commented, the dense vertical bands either side of the step are due to fast capacitance readings, basically ignore unless you want to go down a whole other avenue.
The reason for the tail currents is some channels remain open and close gradually after the step ends "tailing" off. We can't really say what channels these are as we know nothing about the recording conditions/cells involved. However these currents are large, so most likely to be sodium/potassium.

I think I understand the question a little better now. When voltage increased, OP expected an exponential decay but instead saw a peaking to positive value and then going back down to negative value at which exponential decay happens.
Pretty much think of this as two current sources superimposing on each other. One is the current caused by difference in voltage (Ih). Ih is a mix of potassium and sodium current. While it is voltage dependent, it doesn't follow simple Ohm's law as this has to do with activation of channels rather than membrane. source The other is current caused by capacitive property of the membrane. Since capacitive current is proportional to rate of change in voltage, increase in voltage results in positive capacitive current.
So when voltage increased from -125 to -55 mV, there is a positive capacitive current as well as exponentially decaying Ih. These two superimposing each other almost leads to the picture we see in OP's question. I cannot explain why there is the huge negative spike in current after the small positive peak though.
Source: I learned this in class one year ago.
and nice animation of what happens during voltage clamp experiment

This answer doesn't answer the actual question about tail currents and contains several errors. Actually the OP is a better source for what tail currents are from: the channels that are still open and haven't yet returned to the equilibrium at the new voltage.

@BryanKrause do you mind checking to see if there's still errors? More on those errors would be appreciated.

Tail currents are observed because current $I = g(V-E)$ suddenly changes with $V$, whereas $g$ changes gradually following some kinetics. Thus, at sudden transition of voltage $V$, $I$ changes by a factor, which is observed as tail current with a jump.

This is correct and might answer the title question, but it doesn't actually answer the OP. Unfortunately this question has sat for quite some time without feedback from OP and we probably need to get rid of it now.

OP stands for "original poster"/"original post", in this case the question/question asker. Oliver Houston's answer and my comments address the question the OP was actually wondering about, which was the presence of the sharp transients in addition to the tail currents.

How is jump not explained by this ?

If you plug some numbers into the equation in your answer, it would be obvious why you don't get what the OP shows. The paper linked up in the comments by JasonC has an example of what tail currents look like when not impacted by artifacts: http://jn.physiology.org/content/79/5/2345

when you close a switch, an arc of lightning jumps in the air because the voltage rises at that particular point in space momentarily towards a theoretical infinity as the current behind the closing switch places pressure on the edge electrons and force them to jump. that change in voltage is similar to a tail current.


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Can we modify plasmids to eliminate antibiotic resistance?
This is a very general question regarding the potential use of artificially modified plasmids to block or modify bacterial evolution in order to prevent development of anti-biotic resistance.
For example the most crude example might be to modify a suitable plasmid with some gift for target bacteria but also to add a mechanism to block their pili after delivering the gift.
If this general principle was practical, there would be huge scope for ingenious biologists to create a plethora of ideas to modify bacteria is many ways to our advantage, even to the extent of creating completely artificial plasmids for such purposes.
My question is twofold: Is this likely to be a valid approach for modulating bacterial evolution to our purposes, and if so, is there already research in progress in this field?
Of course, in the example above, the gift from the plasmid must significantly benefit the plasmid and the poison mechanism must be delayed long enough for a large % of the biofilm-bound bacteria to be infected by the poison before it takes effect. Also the plasmids must include their own slow-acting poison/fast acting antidote to deal with reproducing cells that do not contain the plasmid. A more subtle approach might be a gift that did not kill the bacteria but modified them to be significantly less virulent.

You can't artificially modify bacteria, decreasing their fitness in an environment containing antibiotics, and then expect them to outcompete bacteria which resist antibiotics.

This will not work since having these bacteria means a strong advantage over bacteria which do not have them, so they will be overgrown.

@Chris Unless the antibiotic in question is currently present, there's no competitive (dis)advantage. Evolution happens without foresight, so it's entirely plausible that a deleterious mutation might sweep a population under neutral conditions. This mechanism is plausible enough that similar mechanisms were (are being?) researched to outcompete wild strains of viruses.

source: Stack Exchange

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

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Book recomendation: cell cycle regulation
I aim to study cell cycle regulation, can some of you suggest a good book or website that systematically explains the topic.
It should include-

Detailed account of Cyclin and cdks involved in different stages of cell cycle
Spindle assembly checkpoint
DNA damage checkpoint
Special roles of Rb and p53 proteins in cell cycle regulation

A) Useless title, again. B) For book recommendations you need to specify with detail what the book should include detail on and why "obvious" choice are unsuitable - as it stands its far to broad/will illicit primarily opinion based answers

Robust texts covering such 4 listed points with rigour include the following selection:

Molecular Biology of the Cell
Molecular Cell Biology
Cell Cycle Regulation
The Cell Cycle Principles of Control.

& even a review of the latter here.
HTH

Start with "Cell Biology" by Gerald Karp (Wiley). You can then move onto "Molecular Biology of the Cell" by Bruce Alberts and Alexander Johnson (Garland Science).

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


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How does the peptidoglycan layer of a bacterial cell wall help prevent osmotic lysis?
I recently read that penicillin works by damaging the peptidoglycan layers of a bacterial cell wall causing osmotic lysis, which is when the bacteria cell bursts due to osmotic pressure.
I just would like to know how peptidoglycan prevents this. Thanks for any responses!

Peptidoglycan is formed by the linkage of molecules of NAM ( N-acetylmuramic acid) and NAG (N-acetylglucosamine) into a polysaccharide structure.  Many of these structures are then formed into a lattice by crossbridges of polypeptides.  In gram + bacterial cell walls many layers of this lattice are stacked up forming a rigid structure, that is external to the plasma membrane, and provides more resistance to osmotic lysis than the plasma membrane alone posesses.
Penicillin interferes with the final linking of the peptide crossbridges which results in a weaker cell wall that will make it more likely that the cell will undergo osmotic lysis.
Gram - bacterial cell walls are quite different than gram + cell walls.  They do contain peptidoglycan but the peptidoglycan layer is thinner - only one, or very few, layers of peptidoglycan with some structural differences also.  Therefore, gram - bacterial cell walls are weaker than gram + bacterial cell walls.
"Microbiology, an introduction" Tortora, Funke and Case 11th EDition pp 84-86

The bacterium always has a higher internal osmotic pressure (they contain a lot of stuff, and most of the time much more stuff than their surroundings). This pressure is contained by the membrane and cell wall, and when you destroy the cell wall the membrane alone is not strong enough, and the bacterium will spill its guts.


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Why do blue jays eat my cat food?
We buy some run of the mill big-box store cat food. Over the last several weeks, I've observed a blue jay landing on the cat food dish, taking a piece or two, and flying off with it. I assumed it was eating it then, and this morning I just saw it actually eat a piece.
Why would a blue jay eat cat food?
Edit:
I just looked at the ingredient list and apparently corn is the first ingredient. But there's also "poultry by-product" and a variety of other "meats." Would the jay just smell a lot of corn or something?

It's food. It's easy to "catch". Blue jays eat insects; why not cat food?

@anongoodnurse But he says it has corn too

@TalhaIrfan - Blue Jays are omnivorous. Easy food is easy food.

Like other Corvids (Jays, Crows, and Ravens), Blue Jays are omnivorous and can eat and digest both animal and plant matter. Animal matter can include insects, carrion, small birds and mammals, and the eggs of other birds. Then there is plant matter including corn, seeds, etc. Your catfood was not only convenient but contains a good source of both animal and plant matter and the opportunistic tendencies of Blue Jays allowed them to take advantage.


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Do I have to chew for digestion to kick in?
Liquid nutrient-rich products (such as Soylent) are consumed without chewing. But if I have to chew to initiate digestion, are those nutrients really "processed"?

If you had to chew to digest, then beverages like sugary sodas would never be digested or provide calories or nutrients, as you (generally) don't chew when you drink them. No, chewing is not required for digestion or nutrient absorption. Chewing is important when eating solid foods, as the chewing action breaks down and begins to solublize the food, and stimulates the production of saliva, which contains enzymes that begin to break down the food prior to digestion in the stomach and intestines.

So digestive fluids are always there, waiting..?

Yes, there is always acid and digestive enzymes in your stomach, and more are produced when food enters it.

what, other than chewing, triggers more acid to be produced upon food intake?

@Sparkler the presence of the food itself. You can read all about the process of digestion here - it is directly linked from the other article I linked in my answer.

@Sparkler Also, saliva production and other digestive enzymes are increased in anticipation of food or from seeing/smelling it.


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Dnase data for GRCh38
This question below turned to be completely faulty. I don't have to do anything with DNase data for GRCh38.
I asked it because of the file count difference between hg38 and hg37, which I thought to be too big.
For hg38 there're 95 files *Peak.txt.gz. For hg37 there're 236 *narrowPeak.gz, but after merging pairs PkRep1 & PkRep2 (probably FASTQ(SE/PE) reps) we get only 123 files. Finally, this difference (123 & 95) no longer seems to be big and we have even cleaner situation without PkRep1 & PkRep2.
One again: there's no problem with DNase data for GRCh38 assembly and only my question was misleading. I'd like to apologise for the confusion I introduced.

I'm interesed in transciptional activity, thus I'm willing to use DNase hypersensitivity sites to detect regions where transcription factors are allowed to bind.
In previous genome assembly GRCh37 / hg19 I used to use narrow peaks files from these two sources (University of Washington and Duke University, respectively) (files with suffixes .narrowPeak.gz):
http://hgdownload.cse.ucsc.edu/goldenPath/hg19/encodeDCC/wgEncodeUwDnase/
http://hgdownload.cse.ucsc.edu/goldenPath/hg19/encodeDCC/wgEncodeOpenChromDnase/
With the most contemporary assembly GRCh38 there're also some annotations attached (files with trailing Peak.txt.gz):
http://hgdownload.soe.ucsc.edu/goldenPath/hg38/database/
And here four complementary question arise:

Consider only datasets, which come from University of Washington.
For GRCh38 / hg19 I counted 236 narrow peak files, whereas for newer
GRCh38 there're only 95 files. How to explain this differene? Do the datasets represent exactly the same coverage, but with much lower granularity / precision (datasets that come for several tissue lines are merged into fewer files)?
With GRCg37 / hg19 we have both narrow peaks as well as broad peaks,
whereas GRCh38 comes with only one type of of file *Peak.txt.gz.
Does it mean that with the newest version we have only narrow peaks? Are the broad peaks hidden somewhere else?
With GRCh37 / hg19 we have two separate sources of DNase data: UofW and Duke. For GRCh38, it seems that only UofW datasets are availabe. Is any other source of DNase data available, maybe stored separately (Duke or other lab)?
Let's suppose that you're in my place and you would like to determine cis-regulatory areas. What type of data can be used to do so? Mabey DNase datasets but from other source or even completly different type of data (NOT DNase)?

Thank you in advance for your answer.

No need to apologize. Your question was very interesting actually and it will aid the future researchers a lot am sure! I would suggest you to revert it to OP

I am unsure that how much does it answer your question, but have a look at the homepage of DeltaSVM - In his work, Lee et al. have used similar datasets (only for GRCH37 I reckon) and I am sure they will address some of your queries.
As you yourself can better determine which dataset(s) are ones you need.


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Why are the human knees and elbows bent in an opposite direction
I can assume that the hands used to be the same as legs. And they got weaken, and changed direction when human started to walk on two?
Also why do the hand palms facing the body and not facing down like the feet?

What research have you done on this so far?

I just found an article talking about god creation, this wasn't what I was looking for. And I still need to read about why human walk on two.

Do you want to know evolutionarily why or developmentally why knees and elbows point in opposite directions? The latter question is more easily answered.

Your assumption is wrong, hands were never the same as legs.

I am no expert on comparative anatomy, but I will give this a shot. Please edit if you know more about this subject!
The configuration of opposing elbow and knee joints is a feature we humans share with large group of mammals. For example, below is an image of a shrew skeleton.

Opposing joints are course a major feature of mammalian anatomy, and there are many studies on its functions and advantages. Among other things, this configuration allows for characteristic gaits of mammals such as the gallop of a horse, and it allows mammals to rest with legs protected under their body. See this page for some basic information.
Neil Shubin's book Your Inner Fish on human evolution also discusses the opposing joints arrangement, noting that this is a "key feature that gives us the capacity to walk, one we share with other mammals". A preview of the book is here.
A quick literature search turns up many technical articles on this subject, such as this review series. I'm afraid the details are beyond me (again, experts please edit), but I think it's fair to say that there is plenty of evidence for advantages of this joint arrangement in mammals.

Good answer+1 Would be great to have answers to the following question: Do we have an ancestor having knees and elbows bending in the same direction? (2) Did joint on forelimbs and hindlimbs evolved simultaneously? Do they use similar metabolic pathway? (Might be worth eventually opening a new post for these)

@Remi.b I'd add any other mammal species, not only direct ancestors.

you can add any other terrestrial vertebrate, not just mammals.

Unfortunately, your question isn't clear. "Why" could mean different things. What course of events led to it? What benefits does it provide? We could just say, it's not disadvantageous this way, so why not. So perhaps you could clarify.
Evolutionarily, through the stages as our ancestors evolved from small mammal to human, the changes that occurred were sufficiently suitable for the species. The joints are oriented well enough for walking, running, and holding things, and there doesn't need to be more reason. As for the hands, they point away from the arms like they do in other great apes. The difference is that in humans, the feet have a hard time pointing down since they are never used as hands, and hands have a harder time pivoting to be perpendicular to the arm because they are never used as feet anymore. Because of these behavioral differences from other great apes, variations that helped feet be used as hands and hands be used as feet were not selected for, but variations that reinforced walking and running ability and that reinforced object manipulation were selected for.

Good answer. What i meant was that i expcted the 4 limbs to be identical since they all were used for walking. But I got already other good answers here that explained it.

@RonenFestinger Okay well then I guess you have your answer. You might also be interested in asking an engineering or mechanics question about it, as tetrapods walking robots often have front and back joints that are mirror opposites of each other. You might also be interested in asking a question of why other animals have opposite front and back joints. What you should keep in mind is that although front and back legs are all used for walking, they don't have identical functions. Back legs might spring more, front legs might pull more and grab prey more.

It's an amazing question, really. And you might be right about your assumption. In the womb, our legs and arms bent in the same direction. But as the foetus continued to develop, the legs and arms rotated to bend in opposite direction (to each other). As of now, there is no rational explanation as to why this happens.
So I guess all we can do is be grateful to the way our bodies have come into being. If, for instance, our knees bent backward (just like our elbows), our legs would bend forward like our arms and we wouldn't be able to walk the way we do. Apply the same to the arms and we'd be lifting things in an entirely different way, and backwards too! Also, we won't be possessing the ability to write.
You can check out this page for more info:https://answersingenesis.org/human-body/your-legs-are-on-backwards/

Thanks. That's what I found too before asking this question. But I was looking for a different answer than god created it this way.

Well I'm sorry I couldn't be of much help, because there is no scientific theory to explain this as of now. You can always do research on it, though.

"there is no scientific theory to explain this" --- this is clearly not true. See my answer for some basic information and pointers.

When exactly are they bent the same way? http://www.parents.com/pregnancy/what-my-baby-looks-like/ And even if they would change orientation in development, that would mean nothing about God, it would mean something about evolution. For example, turtles in development start out with rib cages, like the reptiles they evolved from, and the rib cages fuse into a shell. This is actually evidence for evolution, because if animals were created separately, it would make no sense to make a rib cage and change it later. Please do yourself a favor and un-brainwash yourself with actual science websites.

I arrived here four days ago. And not to parade my belief in God (I don't see life that way), but to get better, more informative answers of scientific questions. So if you think I blindly swallow whatever's fed to me, I'm sorry. I don't. Or else I wouldn't be here. This was my first answer on this site, and now that I'm here, I look forward to add substance to it. And ironically, your link above doesn't happen to be an actual science website either, so kindly practice what you preach. (I don't mean any offense.)


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How would one determine whether a chemical will upregulate a certain class of proteins?
I'm trying to determine whether certain organic chemicals will upregulate classes of proteins that possess deacylase activity.
How would I go about this experiment? I'm assuming I would use some sort of assay but I'm not exactly sure how I'd go about it.

One way of examining this is by looking at the transcriptome as a whole before and after the introduction of the chemical. I would use microarray or next generation sequencing RNA-seq technology to look on the expression level of all the genes after the introduction of the chemical, some inert control and no treatment control.
Then, you can calculate the relative fold change in expression of all genes, under treatment vs. control. Next, you can do a GO term enrichment of the significantly upregulated genes, and see if the term "deacylases" shows significant enrichment in genes that are upregulated under treatment vs. control.


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Stem cell research and female egg synthesis
In terms of years, how far is stem cell research from being able to produce a female human egg from other female body cells?

I suppose that there is no connection between producing egg from somatic cells and stem cell research. The thing that you have mentioned: "produce a female human egg from other female body cells" was already done in 1996 (!) in sheep. Technically, there is no reason that this procedure will not work in Human as well. So in term of years: this was possible 20 years ago ... :-)

Thank you for your answer, but when will it be possible to do this for reproductive reasons and get perfect results, unlike with the sheep where lots of defects emerged from the clones/newborn sheep? Thanks.

This does not answer the question which is about whether egg cells can be produced from somatic cells. What you are describing is SCNT and it is quite a different case.

I see, so what you are actually asking is about reprogramming cells to become eggs?


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Why should phospholipid non-polar tails be "protected" in the membrane bilayer?

lipids are arranged within the membrane with polar head towards the outer side and non polar tails towards inner side, this ensures that the non polar tail is protected from aqueous environment.

My question is why should we protect non polar part ,will it destroy in contact with polar part?
 What should be the correct reason for bilayer arrangement?

Where did you get that quote from? As I mention in my answer, I dislike using the term "protected". It's misleading. Furthermore the quote also uses "inner" and "outer" in an unhelpful way as "inside" and "outside" often refer to compartmentalisation of the cell/organelle/vesicle/thing with a membrane. For example if something is on the inner leaflet of a eukaryotic cell, it's on the cytoplasmic side. The quote in the question would make that sound like it was deep in the membrane.

The issue here is the word protected I think. There is no intentional protection going on, simply the tails are repelled from water (but not each other) and the heads are attracted to water.

What should be the correct reason for bilayer arrangement?

I'll answer your second question first, but there is an almost identical question on this site already: Why do cells have a bilayer?

There is water on the extracellular and intracellular side of the membrane. What's actually happening at a molecular dynamics level is the self-association of the hydrophobic lipid tail groups driven entropically by water. In other words the polar (hydrophilic) head-groups "prefer" interacting with the water (called the interfacial region) and the the hydrophobic tail groups "prefer" not interacting with the water. With those two preferences in play, the lipid bilayer formation we know and love emerges.

why should we protect non-polar part, will it destroy in contact with
  polar part?

To directly address the first part of the question: no, nothing would be destroyed. The word "protect" isn't appropriate (it's a bit too anthropomorphic for my taste!). Here is a video showing the bilayer spontaneously assemble in a molecular dynamics simulation. Read the more thorough 2003 journal article for an idea of early MD simulations of the bilayer formation. As you can see nothing "bad" happens when the water collides with the lipid tails and the lipids aren't destroyed.

Interesting read: MEMBRANE LIPIDS OF THE PAST AND PRESENT. Good animations and explanations of different membrane formations.
For an academic perspective, I'd recommend a couple of reviews: Cournia et al., 2015 and Gerit et al., 2008.


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Where exactly is pleasure
Question from an outsider: have we been able to pinpoint where exactly the feeling of pleasure comes from?
I know that there are several types of pleasure, I'm talking about the 'liking'. If that involves several separate pleasure centers (which is probably the case), I'm interested in any/all of them.
I am wondering if it is the electrical stimulation part, or maybe the release of some chemicals/hormones (but then, where do they go to produce the feeling?), or maybe a chemical reaction somewhere? How much have we been able to narrow it down? Do we know which part of the chain reaction is actually responsible for the feeling of pleasure?
Is it possible to like without a body, just a "head"? Are there experiment on rats (or people) whose body is completely paralyzed?
Any reference to scientific paper, as well as personal opinions or suggestions as to where I could find this type of information would be greatly appreciated.

Well, I'm glad you're curious, but you must realise that your question is highly complex. You'd certainly have to refer to a research paper for the exact, factual information. All the same, I can tell you a bit about Dopamine (the pleasure hormone) based on recent reading.
Dopamine creates pleasurable feelings when it is released in areas such as the nucleus accumbens and pre-frontal cortex. This happens when positive, or rewarding actions are undertaken. Dopamine release in the nucleus accumbens is so consistently tied with pleasure that neuroscientists refer to the region as the brain's pleasure centre. However, this is not the ONLY pleasure centre.
Now this is all I know. You should probably check out this page for more, in-depth info: http://wings.buffalo.edu/aru/ARUreport01.htm
It's a long read, but I'm sure you'll find something worth your time.

In the central nervous system, dopamine is a neurotransmitter and not a hormone. The 'pleasure signal' idea was an old hypothesis that has since been debunked. It's true that nucleus acumbens activation is linked to pleasure, but the case for PFC isn't clear. It would be more accurate to think of dopamine as modifying brain function in response to reward/reinforcement, but not directly responsible for feelings of pleasure. In fact, it can even be released in response to unpleasant stimuli. But, it has many other roles, like low level motor control.

Of course, dopamine has many functions, apart from being associated with the brain's pleasure system. And as far as PFC is concerned, it has been observed that depressed people have significantly low levels of activity in the PFC. Also, I've read in psychology that when we're joyous, activity in the left Prefrontal Cortex is stimulated, so I guess there is a relation. But yes, how far and to what extent does dopamine influence pleasure system is indeed questionable. All the same, thanks for the update on the debunked hypothesis. Feel free to edit anytime.


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Does SIV cause AIDS in primates... If not why
does SIV cause AIDS in primates or have they developed resistance to the virus **

Homework questions and trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. This question can easily be answered by a Google search.

While the question doesn't show much effort, I'm not sure it looks like a homework question - and I certainly wouldn't call it a trivial question (apparently Nature agrees).

From https://en.wikipedia.org/wiki/Simian_immunodeficiency_virus:

Unlike HIV-1 and HIV-2 infections in humans, SIV infections in their
  natural hosts appear in many cases to be non-pathogenic. Extensive
  studies in sooty mangabeys have established that SIVsmm infection does
  not cause any disease in these animals, despite high levels of
  circulating virus. However, if this virus infects an Asian or Indian
  rhesus macaque, the animal will develop simian AIDS (SAIDS).[5] A
  recent study of SIVcpz in wild living chimpanzees suggests that
  infected chimpanzees experience an AIDS-like illness similar to HIV-1
  infected humans. The later stages of SIV infection turn into SAIDS,
  much as HIV infection turns into AIDS.

Later in the article:

Beatrice Hahn of the University of Pennsylvania and a team of
  researchers in 2009 found that chimpanzees do die from simian AIDS in
  the wild and that the AIDS outbreak in Africa has contributed to the
  decline of chimpanzee populations. Testing wild chimpanzees,
  researchers detected organ and tissue damage similar to late-stage
  human AIDS. The infected chimpanzees had a 10 to 16 times greater risk
  of dying than uninfected ones; infected females were less likely to
  give birth, could pass the virus to their infants, and had a higher
  infant mortality rate than uninfected females.

A couple of key references:
Keele, B. F. et al. "Increased mortality and AIDS-like immunopathology in wild chimpanzees infected with SIVcpz" Nature 460, 515-519
Commentary on the above: Hayden, EK (2009) "Wild chimpanzees get AIDS-like illness" (DOI: 10.1038/news.2009.711)
Heeney J, Dalgleish A, Weiss R (2006) "Origins of HIV and the evolution of resistance to AIDS" Science 313(5786): 462–466


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For a recombinant pUC19 plasmid with cut sites at Hind III and EcoO109i, does lactose need to be present for the gene of interest to be expressed?
I am growing E. coli transformed with the plasmid pUC19 with an insert of an enzyme in rat brain between the mentioned cut sites (EcoO109i and HindIII). I have isolated and created the recombinant molecule with custom gene synthesis so that the gene encoding for the enzyme easily ligates into the plasmid.
It is after the lac promoter and lac operator, so will I need lactose in the growth media for the enzyme to be made?

Why would you cut out the entire lacZ operon instead of using the MCS? Without any of the machinery expressed from the operon, who knows how well expression of your target gene will work?

@MattDMo lacZ is a single gene, not an operon. The only negative effect I can think of (assuming there are no issues from removing the fragment between lacZ and ampR) is the inability to do blue-white screening with the plasmid.

I would rather use the synthetic analogon IPTG for induction of genes behind a lac promoter, as they are not getting degraded (or at least much slower than lactose) and thus give a much stronger induction signal.
You will need to test the optimal IPTG concentration, but as a starting point I would use and endconcentration of 1mM. If this is not optimal (to much unsoluble protein or not enough), you can change the concentration in either direction. To start, use an overnight culture to inocculate a fresh culture in the morning and follow up the OD600 until it reaches 0.6-0.8 before adding the IPTG.


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Nerve endings on the skin
We can perceive sensation of pain if we are poked on any part of the skin.  Does this mean there is a nerve ending at every point on the skin?
Does this also mean that each of these nerves go all the way to the brain as single strands so that the brain can distinguish between the touch at any two distinct locations?

Could you? I don't believe you can. Try blindfolding yourself, have a friend poke you with a sharp pencil, then you try and mark the exact spot (after the pencil has been removed) with an ink pen or Sharpie, then have the friend tell you how close you were, or take an image before the pencil indentation fades.

Testing this is a common experiment given to public-school children; described here for example.  As that link shows, threshold distances vary widely over the body, with few regions being remotely as sensitive as the question asks.  Since the premise of the question is shaky, you may want to revise it to focus on the question you want answered.

@MattDMo - Hope the question is now valid


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marine animal tracking databases
Which databases you know that store data on tracking of marine animals?
I am interested particularly on mammals (for which I know meop storing data on sea lions) but also on fish schools (not sure they exist though).

could you explain what sort of information you need in more detail

I am interested in spatial tracking. Track animals' movements and vertical movements

One major tagging effort/database is the TOPP program-- "Tagging of Pelagic Predators". They track Pacific Blue Marlin, Mako Sharks, Whale Sharks, Salmon Sharks, Pacific Bluefin Tuna, White Sharks, Atlantic Bluefin Tuna, Northern Elephant Seals, and Leatherback Sea Turtles. I'm not sure if their data are publically available.
Info here: http://gtopp.org/ and here: http://oceanview.pfeg.noaa.gov/TOPP/

WhaleNet is less pretty, but has older marine mammal tracking data: Gray Seal, Harbor Seals, Harp Seals, Harbor Porpoise; dolphins (archived) and whales (archived): http://whale.wheelock.edu/whalenet-stuff/stop_cover.html

Sea turtle tracks can be found at http://www.seaturtle.org/tracking/

Check out MoveBank.org. It provides access to online animal tracking data (whales, turtles, seabirds, etc.). Some come with ancillary data like depth. Best of luck!

The Animal Telemetry Network (ATM) was "established to provide unity, stability and continuity to the national infrastructure that facilitates the collection, management and availability of this marine animal telemetry data. To accomplish its mission, the ATN is being implemented in three Phases and on these three foundational pillars: 1) Building Alliances and Collaborations, 2) Providing Telemetry Data Aggregation, Management, Display and Delivery, and 3) Funding High Priority Regional Baseline Animal Telemetry Observations." The network provides access to maps with data, will sometimes provide links to publicly available data, and provides point of contact for each dataset.

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


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"Most bacteria have at least one cell wall"
In the first answer to How do we find antibiotics? @Ashafix claims that

Most bacteria have at least one cell wall

Does this mean that there are bacteria with more than one cell membrane? Which are those and how does that look/work? Are there different milieus in the different compartments?
Cheers

Thanks! I will edit the original answer accordingly to make it more clear.

The phrase you quote is a little unclear, but in looking at the page you link to I believe that @Ashafix was referring to Gram-positive (one cell membrane) and Gram-negative bacteria (two cell membranes).
Each type has only one cell WALL, which refers to the structural peptidoglycan layer, which is between the two membranes in gram-negative bacteria, and is much larger in gram-positive bacteria.
The differences between these two cell types are of some interest with regard to the biology of what structures can sit in the cell membrane and how easy they are to work with in the lab, and how easy things are to get across the cell wall (w/r/t @Ashafix's original point).

Thanks, @Maximilian. Yes I got the original point of the refered to question. I was merely wondering just that which you answered. Thanks. As I'm only just signed up of this community, the only thing I can award you is the checkmark. Sorry.

great, glad that it got cleared up. no worries on votes or whatever.

I agree with @Maximilian that the phrase you quote is unclear, and we can't understand if it's talking about the number of cell walls of about the presence of cell walls:

Most bacteria have at least 1 cell wall, meaning that some bacteria can have more than 1

This is wrong, as @Maximilian explained. But this:

Most bacteria have a cell wall, meaning that some bacteria doesn't have any

Is correct. Tenericutes, a group of Eubacteria, don't have cell wall:
http://onlinelibrary.wiley.com/doi/10.1002/9781118960608.pbm00025/abstract
Reading the answer, it's clear that the user was talking about the outer membrane in Gracilicutes.
However, it's good to emphasize that all bacteria have only 1 cell membrane, because the outer membrane is not defined as a "cell membrane" (despite being a phospholipid bilayer): http://www.nature.com/nrmicro/journal/v13/n10/images/nrmicro3480-f1.jpg

Also enlightening. I wish I could up you as you deserve. As I commented on the answer above: I cannot award an up-votes due to lack of reputation of my own, but thank you very much for your interest and care.

No worries, mate! And good on you for giving @Maximilian the checkmark, a lot of people in SE communities ask the question and simply disappears after getting the answer.

Well, how fun can it be to help those people when they ask their second question? It makes me glad and grateful that you people are around and give of your time and share your knowledge. That goes for all on SE that answers and discuss. @Maximilian too.

+1 @Gerardo, looking back I believe you have the right of it.


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Does RNA-LPX expression of antigen by DC induce only T-cell with that antigen specificity?
There was a recent publication concerning use of IV administered RNA-lipoplexes with an adjusted electrical charge to encourage dendritic cells (DC) to pick up the RNA package encoding viral or mutant neo-antigens, for example, a sequence of melanoma tumor cell coded to RNA. The paper is at Systemic RNA delivery to dendritic cells
After reading that abstract and related papers (see Dendritic Cells Pulsed with RNA are Potent Antigen-presenting Cells In Vitro and In Vivo By David Boczkowski et al I came away with the concept that the RNA segment of encoded tumor protein was taken up by a DC and the DC translated that to a protein (antigen) that it presented with MHC of the appropriate class (class I I believe in these tests) to a naive T-cell, which would subsequently amplify and pursue and kill tumor cells with that antigen (by becoming CTL cytotoxic T cell leukocytes).
A quick look at my immunology text from NIH tells me that this mechanism (DC's bringing antigen to naive T-cells in lymphatic tissue) ensures "that rare antigen-specific T cells will encounter their specific antigen on an antigen-presenting cell surface."
My question is does this mean that the so-called "mutant neo-antigen" of a particular tumor in an individual must still find a T-cell receptive to that sequence (epitope) at least in part (say fractionally)? I guess I'm wondering whether there might be the case where a particularly diabolical tumor presented such novel sequences that no existing T-cell rare or otherwise could be receptive to a fraction of its sequence (even when a customized RNA delivery of a selected portion of the sequence was delivered via DC to the T-cell).

After I posted this I looked at link and more or less answered my question. I gather I'm supposed to wait 24 hrs before answering my own question. Preview: Computer methods are used to identify sequences from a tumor mutanome that are likely to express non-synonymous protein present in a peptide presented on MHC molecules, so it is likely at least one mutated epitope would be immunogenic (T-cell druggable).

The OP (me) was unclear whether or not the new therapy had to ultimately present antigen specific to a particular naive T-cell. The answer is yes: Each T-cell is specific for a single antigenic determinant. An antigenic determinant is a small portion of an antigen, such as a certain sequence of amino acids in a protein, that the immune system (a T-cell receptor in this case) recognizes as non-self or altered self. The antigenic determinant is also known as an epitope. Typically an antigen has many different epitopes, each able to react with a specific antibody or T-cell receptor (when presented with MHC).
The confusion arose from the description of the RNA as encoding "mutant neo-antigens" (among other possibilities, e.g., viral or endogenous self-antigens). At first glance this seemed to imply that a tumor antigen constituting a novel polypeptide antigen ("mutant neo-antigen") was able to induce T-cell response (effector and memory T-cell responses) in the absence of any T-cells with a T-cell receptor specific to that neo-antigen. That would not be possible.
Through somatic gene rearrangement in development, T-cell receptors (TCR)  have a wide range of antigen specificity, such that each T-cell has a unique receptor on its surface able to recognize foreign protein antigen associated with MHC molecules. Some estimate that human TCR and antibodies can respond specifically to 10 million different antigens.
Apparently the distinction is made between classical tumor-associated antigens that typically constitute autoantigens (which may appear frequently on the surface of cancer cells in conjunction with MHC and therefore generate some antibody response, possible ineffective) and neo-epitopes, the latter being the result of the estimated 25 – 30% of antigenic mutations (mutations not normally found in the genome) in tumors that could be made to induce immune response on the single- or poly-epitopic level. It appears that autoantigens are more modified normal protein that tend to appear somewhere in the disease process on a particular class of tumor than the result of entirely novel mutations. Since tumors usually have tens to hundreds of non-synonymous mutations, the mutanome of a tumor provides many possible targets for custom poly-epitope vaccines for each individual patient. Coding messenger RNA (mRNA), i.e., synthesizing mRNA to encode multiple transcripts for synthetic poly-epitopic nucleotide sequences, is an attractive antigen delivery format.
In order to locate a sequence that would be likely to act in this capacity (that is, to select tumor mutations likely to exhibit immunogenecity), an approach like the following serial selection has been suggested: (1) next generation sequencing (NGS) of an patient's individual tumor mutanome and patient genome (2) identify triplicate sequences present in the tumor mutanome but not in the patient genome, i.e., identify the mutations in the tumor that distinguish it from normal self (3) identify those mutations that are likely to code for a protein (4) identify those mutations that are likely to cause a non-synonymous protein change (5) identify those mutations meeting all the previous criteria that a predicted to be in a peptide presented on tumor MHC. An example quantifying this selection process is that of the murine B16F10 melanoma mutanome: The NGS exome profile (coding exons) predicted 12,842 mutations; 3570 of those predicted as somatic mutations; non-synonymous mutations 962; mutated peptide predicted to bind MHC 462; 50 of those selected for testing and of those 50, about a third of those tested strongly immunogenic when encoded to RNA and transfected to dendritic cells, i.e., inducing strong T-cell response. As a test of actual anti-tumor effect, mice were immunised with the encoded mutations identified and achieved complete tumor protection and survival in 40% of the group, compared with death of all control group animals.
Generalizing, a poly-epitopic vaccine formed from a tumor mutation should be selected to be specific to the tumor and not in the patient germline genome, to occur in a protein-coding transcript, to cause a change in protein sequence and that protein be expressed in tumor cells. In order for the mutation to induce a robust T-cell response, the mutation-containing epitope must be presented on the patient's MHC molecules in the dendritic cells during vaccination (and at least one T-cell must possess a receptor specific for one of the epitopes) and in the tumor cells for recognition (on the surface of the tumor cells). With the patient HLA haplotypte, MHC-binding epitopes can be predicted with computer algorithms. The immunogenecity of the computationally predicted epitopes can be tested in vitro with T-cell stimulation.
One of the challenges to RNA delivery has been degradation by ubiquitous extracellular RNAses. The study noted [Systemic RNA delivery to dendritic cells] solves that issue by protecting the RNA with lipid carriers to form RNA-lipoplexes (RNA-LPX). This has the additional adjuvant effect (the RNA-LPX) of triggering interferon-a (IFNa) release by plasmacytoid DCs and macrophages in a manner similar to early phases of viral infection.

I would hesitate to say the liposomes "solved" the problem of protecting the RNA in circulation. It definitely helps though. mRNA delivery is a pain, but the study here probably benefited from liposome formulation's tendency to accumulate in liver and spleen. All of these nanoparticles tend to accumulate in those organs.

@user137 Good point. I just read Sahin's 2013 patent application at https://www.google.com/patents/WO2013143683A1?cl=en and that did make clear the difficulties you allude to, although Sahin's method of creating nanoparticle liposomes with electro-neutral or slightly negative charge apparently targets the spleen preferentially over other organs. This is the desired end if you want to get an RNA antigen payload to professional APCs without damaging other organs like the liver and lungs. Thanks for the clarification.

@user137 ...and the Sahin neutral or slightly negative liposomes seem to have some of the advantages of PEGylation in decreasing the RES (reticuloendothelial system) clearance of lipoloplexes from blood, which may have been more of the central thrust of your comment, i.e., that nuclease degradation (protected by lipoplexes) is only one component of the problem of protecting the RNA in circulation (so I was indeed a bit optimistic earlier).

As of December 22, 2020 both the Moderna and Pfizer RNA vaccines for the original COVID-19 are carried by lipid nanoparticles with PEG (polyethylene glycol). One can only hope they can move quickly with the UK variant that has just appeared with modification to the spike protein that is targeted by these two RNA vaccines.


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What is the difference between natural selection and adaptation?
From what I've read it seems that the only actual difference is that creationists use adaptation and people who believe in evolution use natural selection. But otherwise, from my understanding, the two terms are synonymous. Is that correct?

No offense but I would love to down vote @InstructedA 's comment. (A) There are plenty of religious believes but (1) it is not our job on a science website to make a review of such beliefs and (2) your view of creationist believes is unclear and IMO wrong in the same time. (B) While believing in god (theist) or not (atheist) is correlated in accepting the theory of evolution, one can accept the theory of evolution and be theist or refuse to accept the theory of evolution and be atheist as one domain is about science while the other depends on an ideology.

Always for @InstructedA  (C) It is very obvious from your comment that your understanding of evolutionary processes is very limited. (D) Point "B" above is a discussion of philosophy and not biology. Point "A" above is a matter of religious studies and not biology. These topics are interesting, please open a post at the convenient location to discuss such topics.

I've been teaching evolutionary biology for more than 20 years, and I don't believe in evolution (and I never will). As Tertulian once said, one believes in absurd things. Science is a matter or knowledge, not believing.

The down vote is not a punishment but a help for other's to recognize good from bad info. Scientists don't believe in "absolute facts" whatever that means. Natural science does not "prove facts" anyway but only offer series of evidences congruent with a hypothesis. Anyway, this is not a place to discuss that. You might want to have a watch a short introduction to philosophy of knowledge and philosophy of science. I am not going to answer further comment in this inappropriate place.

I am glad that it is not a punishment, as I see and recognize massive amount of inconsistencies in the theory of evolution the way it is being presented. When I was young I was like you, but then the 'church' presented me with a much better theory. Things are so consistent. I have always hoped that the 'scientists' can provide their alternative remedy, but all I got was 'you are stupid, you are empty'.

Natural selection is a mechanism that is used for adaptation. With only selection and no generation of variation the adaptation is highly limited.

Natural Selection
Natural selection is the differential in survival and/or reproductive success among different individuals. As such, natural selection also refers to the process by which genotypes associated with greater fitness increase in frequency in the population through time.
More information on wikipedia > Natural Selection
Adaptation
An adaptation (or an adaptive trait) is a trait with a functional role that evolved (and is maintained) by means of natural selection.
More information on wikipedia > adaptation
Usage
Both the terms adaptation and natural selection are extensively used in science (and none of them come from the creationist religious belief). Their definitions are related as one is causing the other but these terms are not synonyms.
Further information
As the question is very introductory in the field of evolutionary biology, you might want to have a look at an introductory course to evolutionary biology. Evolution 101 (a.k.a. Understanding Evolution) by UC Berkeley is short, concise and very accessible even for those that have little a priori knowledge in biology.
Side Note
You said "believe in evolution". It is of course a common phrasing from the creationist ideology. Evolution is a theory (a theory is very different from a hypothesis see this answer for more information) and therefore, the phrasing "to believe in evolution" sounds quite wrong as it wrongfully suggests evolution is a thing on which we could legitimately have different opinion about its existence.

Great answer. To make things worse, in my language (and I reckon than in English too), the students use adaptation both as a noun and as a verb (to adapt), confounding it not only with "selection" but also with "evolution".


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Parafilm vs Foil for Retaining Plate Moisture while Allowing Gas Exchange
We often plate Streptomyces aureofaciens and grow them in a 30°C room. A post-doc I work with has always loosely wrapped the agar plates in aluminum foil to retain moisture and prevent cracking of the agar media over extended culturing periods (up to 21 days). Another graduate student is saying that parafilm would be much better as it allows gas exchange. The post-doc agrees that parafilm would retain the moisture, but also believes the parafilm will starve the cells of oxygen over time. The parafilm we use has a reported oxygen permeability of 150 cc/m2/24 hours. I don't really know how much oxygen a plate of streptomyces would consume over a day. Thoughts?

Oxygen consumption depends on the growth rate (and vice-versa). If it takes very long time to culture the organism, then it probably doesn't consume oxygen that fast. Parafilm is a better choice than foils but I am not too sure about its gas permeability. As tweaks, you can use a bigger container for culturing or use a humidified incubator.

This may be a problem that is easier to solve by experiment than anything else. Make a set of cultures with parafilm and compare to a parallel set with foil. If the parafilm cells are fine, everything should be ok. If you get a significant difference in cell number or viability or something, then parafilm might not be ok. As a benefit, parafilm is cheap, so this shouldn't be a difficult experiment.


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What fruits will naturally ferment?
If left unpicked after the fruit ripens, what fruits may ferment instead of just rotting? My perception is that most fruits just rot.
I know figs will ferment. I'm guessing that this is because the wasp that pollinates the fig carries yeast inside what will become the fruit.
Eating ferment figs got me thinking about how humans first discovered ethanol. I'd guess that they ate ferment fruit and fiddled around until they could reproduce the process.

basically any fruit Yeast is everywhere. its more about conditions than type of fruit.

First, before talking about fruits, let's remember that fermentation is an energetic metabolic process where there is no net oxidation of the substract. Bacteria, fungi, animals like you and me and even plants can use fermentation in different occasions. Plant cells, like fungal cells (and unlike bacteria and animal cells) perform alcoholic fermentation. So, there is no need of a fungal contamination to make a plant tissue producing ethanol.
But, of course, the presence of fermenting fungi, particularly yeasts, can make alcoholic fermentation much faster and noticeable. Several fruits contain what is called "ambient yeasts" (differing from "cultured yeasts", which we add to the fruits latter) covering them, and I believe the most famous example are grapes. Grapes are covered by several genera of Ascomycota (like Candida and Pichia), which can lead to alcoholic fermentation of the fruit. These species are different from Saccharomyces cerevisiae, the most common "cultured yeast" (and the one used in winemaking), but they can produce ethanol the same way.
This "natural fermentation" of grapes is known for a very long time, and it's probably one of the first cases of natural alcoholic fermentation known by civilized man.
EDIT: references for alcoholic fermentation in plant cells:

http://www.plantphysiol.org/content/149/2/1087.full

Under oxygen-limiting conditions, pyruvate can either be converted into ethanol by pyruvate decarboxylase (PDC) and alcohol dehydrogenase (ADH) or to lactate by lactate dehydrogenase.

http://www.plantphysiol.org/content/100/1/1.full.pdf+html

During the early hours of germination [...] seeds rapidly generate high respiratory quotients and exhibit increased ADH2 activities and active alcoholic fermentation.

Hi Gerardo. Can you please give an example along with a suitable reference for alcoholic fermentation by plants? It is an interesting point and a reference would allow users to learn more about it.

Thanks. I was really talking about getting a relatively large amount of fermentation. So the fruit would need to be high in sugar. Grapes fit that need well.


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How do normal cell division chance into a tumor forming cell division?
Or its better to say what happens at molecular level that tumors are formed?
I tried normal google search and google books but couldn't find any appropriate explanation.
I am trying to understand why p53 or Rb genes are called tumor suppressor genes.I'm acquainted with the pathway through which p53 protein cause checkpoint arrest if the DNA is damaged and the pathway through which pRb protein cause G1 arrest.

In a word: mutation.
If you step back and think about it, multicellular organisms are really, really complex systems. Different cells have to do different kinds of things and interact with each other, they form organized tissues and organs and so on. That much is obvious.
For all of this to work in concert, cells have to grow and divide (to replace dying cells) in a nice orderly fashion/at a nice orderly pace. Since that's a complicated process, lots of the genes in any given cell play a role in managing how long that cell lives/how fast it divides (i.e., cell cycle regulation).
So now, if DNA in a given cell gets mutated, there's a chance that mutation will hit one or more of these genes that are involved in cell cycle regulation. And you can imagine there are two extremes of what might happen: On one extreme, the mutation could mess up the cell cycle in such a way that it's broken (the cell can't grow/divide, things get screwed up, and it dies off); on the other extreme, the mutation could instead destabilize the cell cycle in such a way that it's "kicked into overdrive."
In the first example, we wouldn't observe the effect; the mutated cell would just die off, no big deal. But in the second example, with the cell cycle in overdrive, that cell would barrel ahead, growing fast and dividing faster than the cells around it. And since each of its child cells would have the same DNA and thus have the same "kicked into overdrive" mutation, they'd divide too quickly as well, and so would their children…and eventually you'd have a crazy mass of out-of-control cells. That's a tumor.
p53 is a tumor suppressor because it effectively "sounds the alarm" when it notices DNA damage (mutation)—meaning, when it finds DNA damage, it initiates several processes to try and control/fix/stop it. This is important because if that DNA damage is like the second example above, it could lead to a cancer that harms or kills the whole organism.
If the p53 gene itself is mutated, then the cell has lost one of its major defenses against damaged DNA, and thus there's a much greater chance that a cancer-causing mutation in some other gene could go unchecked. That's why damaged p53 is found in lots of cancers: because the cell lost a big defense mechanism against cancer, and then cancer happened.


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difference between motifs, domains, patterns, signatures and profiles
I can't get clear the difference between those terms, I see them a lot while browsing on Prosite, Pfam, Expasy e.t.c.
However, I can find documentation about them, but It still not clear what the difference is between those terms. I think it's something like:

motifs: Short residu stretch, not an indication of homology
domain: Could contain motifs, howevever most of the time is bigger, it can be used to identify homology if two proteins share a domain.

However I can't fit the patterns and profiles in this list.

Looking at the documentation you provide, I think that I can provide definitions for those terms as defined by EXPASY. Note that those definitions may just be an in-house system that EXPASY uses that you can't generalize to other databases for instance.
First, in section I.C of the documentation, they write "The use of protein sequence patterns (or motifs) to determine the function(s) of proteins is becoming very rapidly one of the essential tools of sequence analysis."
So it looks like for them patterns = motifs and motifs = patterns. Note again that "pattern" appears to be a somewhat informal term. I would certainly say that it is confusing that they use them as synonyms, but they do at least define them as such.
Second, I think that they are using the word "profile" in a very narrow technical sense, with regard to the way that they detect homology between proteins. The standard way to detect homology between proteins is using programs called Hidden Markov Models (HMMs). In section II.B, they write "A profile or weight matrix (the two terms are used synonymously here)...". So a profile is really just a weight matrix derived from a HMM that can be applied to any given alignment to figure out whether or not it matches homology. They go on to give an example of how this weight matrix is applied.
In simple terms, how the HMM works is that you give it a bunch of sequences that you know belong to the same family, and it will try to learn the frequencies of amino acids at each position and what order they come in. This model of the amino acid frequencies is the weight matrix they talk about. Then you make sure that the HMM works well (gives high scores for proteins in the same family, low scores for proteins in different families), and then you can apply the program to try to find new homologs.
Hope that answers the Q.

Thankyou, however It's not really clear what the difference is between patterns and domains? Because domains are also used to determine homology? @Maximilian Press

@Rick Beeloo, the scope of the question appeared to concern the definitions of profile and pattern. Nonetheless, the answer may be found again in the docs: "There are a number of protein families as well as functional or structural domains that cannot be detected using patterns due to their extreme sequence divergence; the use of techniques based on weight matrices (also known as profiles) allows the detection of such proteins or domains." So it seems that the domains are identified using the patterns/profiles.

I think it's like this:
signatures:

domains (which are detected using profiles)
motifs = fingerprint = pattern

Where motifs are short stretches of residu's which can be part of a domain, but don't have to be part of it.
Domains are functional unitits of a proteïn (which thus can contain motifs).

this is what you mean? @Maximilian Press , I couldn't wirte a structured summary of your answer so I wrote a new answer. However I will check yours as the problem solver don't worry

yes, I believe that is right- sorry, for whatever reason I was not alerted by this newer comment.


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Number of Chromatids in G1
I know that in G1, the number of chromosomes is 23 pairs, so 46.
I assumed there were 46 chromatids too.
Why is the number of chromatids in G1 actually 0, not 46?
Thanks.

These terms are quite similar and, for many, confusing:

Chromatin
Chromosome
Chromatid

But they are not synonyms. According to Molecular Cell Biology, Lodish, 4th ed:

Chromatin: Complex of DNA, histones, and nonhistone proteins from which eukaryotic chromosomes are formed.

Which brings us to:

Chromosome: In eukaryotes, the structural unit of the genetic material consisting of a single, linear double-stranded DNA molecule and associated proteins.

So, you can think of chromatin as the building material of chromosomes.
But chromatid has a very different definition:

Chromatid: One copy of a duplicated chromosome, formed during the S phase of the cell cycle, that is still joined at the centromere to the other copy; also called sister chromatid.

So, one should not use the term chromatid as synonym of chromosome. Chromatid is the name of each copy of the chromosome after the S (synthesis) phase. According to that terminology, there is no chromatid before the duplication.
I have to confess that I personally don't follow that terminology: I like to say to my students that, before S phase, each chromosome has 1 chromatid and, after the S phase, each chromosome has 2 chromatids. Even this not being the most correct terminology, it has some advantages: it makes the student understand that the number of chromosomes doesn't double after the S phase.

Source:

Lodish, H. (2002). Molecular cell biology. 4th ed. New York, N.Y.: Freeman

Classic example of too many names spoiling the meaning.


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What's the correct name for the war of sexes in evolution?
I'm searching for the correct term for the part of the selfish gene evolution regarding sexes. In nature, this means the evolution of the traits such as the ducks' adaptation to "trap" the drakes' penises in order to restrict the male from attending to other females.

Sexual dimorphism  (?)

The correct term is sexual conflict (but if you see my answer you will see that sexual dimorphism is related) @SciEnt

Sexual Conflict is the word you are looking for!
Sexual Conflict occurs whenever the optimal mating strategy for the female and the male differ. For example, in Drosophila, it is beneficial for a male to mate as much as possible, while it is beneficial for a female to mate only a few times.

That's true of most species, where reproduction is extremely energy costly -- compared to insemination.

I would like to expand a little on Remi.b's answer and point out that there are two key forms of sexual conflict.
Sexual conflict arises when the sexes have different routes by which they maximise fitness.
In the case of the ducks (and many other species) the males increase fitness by mating as much as possible, whereas females may optimise fitness by slowing the males rate. These sorts of conflict where behaviour or phenotype of one sex is beneficial to one sex and harmful to the other is called interlocus sexual conflict: the effects of one locus have consequences for other loci. The bed bug is a fantastic example of coevolutionary dynamics between the sexes resulting from interlocus sexual conflict - males use traumatic insemination and females appear to have made multiple adaptations in response.

"In inter-locus sexual conflict, the sexes experience opposing selection pressures on one or more traits, but the genes affecting the expression of the trait probably differ between the sexes."

Alternatively there is intralocus sexual conflict; when the evolutionary interests of either sex differ within loci. In this case selection favours different alleles in either sex. Genetic covariance needs to be reduced for the sexes to be able to move towards their own phenotypic optima, with such sexually antagonistic selection leading to sexual dimorphism when covariance is reduced.

I wasn't aware of these terms. Was worth expanding on my answer +1


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Using only one antibody to detect COX-2 enzyme
If I wanted to detect COX-2 from a western blot test, would only a primary antibody work? I'm on a budget so does anyone know of relatively cheap COX-2 antibodies?

Considering that you would need to conjugate the primary antibody to HRP or fluorophores (depending on what detection method you're using), it may well be cheaper to use a secondary antibody.

Unfortunately, you'll often find a relationship between cost and quality in antibodies. Sure, there's lots of cheap Abs on the market, but is it really worth saving $50 on the Ab if you have to repeat your western 6 or 8 times to get an image-quality result? I used to do tech support for a reagent company, and I've heard lots of stories....


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Can I tell my antioxidants intake based on nutrition facts labels?
The recommended daily intake of fruits and vegetables is 5-10 portions (url), in order to meet the "required antioxidant levels" (dark-leaf green vegetables, berries, cruciferous vegetables, ...).
Can I measure my antioxidant intake based on nutrition facts label, instead of counting vegetable portions?
Adding up the total intake of vitamins A, C, E and magnesium may not be representing because they are not necessarily the "major players" (additional significant players are CoQ10, alpha-lipoic acid, l-carnitine, acetyl-l-carnitine, n-acetyl cysteine).

What do you mean by "major players" ?  Vitamin C (ascorbate) is certainly considered a quantitatively important antioxidant; it is perhaps the most important soluble radical scavenger in mammalian cells. But in many cases, including the metabolites you mention, I think the quantitative important is unclear.

Also, in your original post your specifically asked about vitamins A, C and E. Now it seems you have revised the question to indicate that you don't care about those vitamins.

@Roland I do, if they are significant "players"; updated question.

See revised answer. I don't think it makes sense to think about this in terms of "major" or "minor" players. The relevant distinction is between vitamin compounds, which are required in the diet, and non-vitamin compounds which are not (by definition).

Well yes, you could get this information from food labels, since the recommended daily intake of vitamins is well established. But there is really no need to worry about dietary "antioxidants" (usually vitamins A, C and E, and carotenoids). If you eat a reasonably balanced diet, you are getting all the vitamins you need. Thankfully, vitamin deficiency is very rare in the western world today.
There is a lot of hype around "antioxidant" dietary supplements, but there is no convincing evidence that high levels of these vitamins in your diet has any beneficial effect at all. Randomized clinical trials have failed to show any effects whatsoever of antioxidant supplements on chronic diseases, and excess intake may even increase overall mortality.
Non-vitamin compounds like carnitine are not necessary in the diet at all, since they can be synthesized by the body in sufficient amounts. In general, the fact that a compound is a "major player" in cellular metabolism (in oxidative defense or other wise) does not mean that you have to consume it. For example, the TCA cycle intermediates are arguably the biggest "players" in human metabolism, but none of them are necessary in the diet.

+1 for showing evidence that dietary antioxidants are a waste of time and money

@Sparkler  I revised your edit and added a reference for overall mortality; there is no evidence for a beneficial effect in this measure either.

What about antioxidants that cannot be synthesized by the body and that are not tracked by the nutrition facts label?

There are no known essential antioxidants outside the 13 vitamins. Some minerals like Selenium are required by enzymes involved in antioxidant defense, but these are already included in the recommended intake scheme.  Of course there are many pharmacological compounds with antioxidant properties that do not occur normally in the body, but that's a different story.


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Output of clustalo on (1.2.1) on ubuntu 14.04
I am trying to align the following 8 sequences using clustalo on ubuntu terminal using the following command. But I am not getting the right output.
clustalo -i sequence.fasta -o output.clu

My input file issequence.fasta with 8 sequences I downloaded from BLAST
My output file output.clu

The output I was hoping for outputOnline.clustal
Also I would appreciate if some can tell me how to share this kind of data in a question because obviously the way I have done is doesnot seem appropriate.

You just need to specify the output format with the outfmt flag.
clustalo -i sequence.fasta -o output.clu -outfmt=clu

should give you the desired output.

How to share data?
Try using an abbreviated example which people can copy&paste, for longer data you could use something like http://pastebin.com/ but the URL might expire.

gi|1709777|sp|P51780.1|PRIO_TRIVU MGKIQLGYWILVLFIVTWSDLGLCKKPKPRPGGGWNSGGSNRYPGQPGSPGGNRYPGWGHPQGGGTNWGQPHPGGSNWGQPHPGGSSWGQPHGGSNWGQGGYNKWKPDKPKT
gi|1709773|sp|P52114.1|PRIO_MUSPF MVKSHIGSWLLVLFVATWSDIGFCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQWGKPSKPKT
gi|1709774|sp|P49927.1|PRIO_PIG MVKSHIGGWILVLFVAAWSDIGLCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQWNKPSKPKT


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Why is oxygen and CO2 measured in pressure instead of mmoles/L like other ions?
Na, K, Cl...All measured in mmol/L in plasma. Why is oxygen and CO2 measured in pressure (mmHg)? (I guess it has something to do with them being bound to RBC but I don't know why the difference).

By the ideal gas law, PV = nRT, you can find pressure by dividing both sides by volume, P = nRT/V. Since R is a constant, and you can usually assume T isn't changing very quickly for biological systems, you can pretend P = n/V, which is moles per unit volume, analogous to concentration. The reason the units are written in pressure is probably because gases are hard to weigh, but measuring pressure is easy. This also accounts for the affect of temperature, which shouldn't affect the soluble ions you mentioned, but would affect the "concentration" of gases.

@user137 Good answer. Could you make it into an official answer

As you suspected, hemoglobin is the reason why O$_2$ and CO$_2$ in blood are expressed as a pressure (mmHg) and not a concentration. Most of the oxygen in blood is bound to hemoglobin; the concentration of free oxygen in plasma is low because oxygen does not dissolve well in water (which is of course the reason why hemoglobin exists in the first place).
When the oxygen content of blood is given as a pressure, it refers to the partial pressure that a gas (air) must have in order to be in equilibrium with the blood. This might seem a bit roundabout, but it captures the effects of both solubility and hemoglobin. In essence, this pressure describes how much oxygen the blood can release, which is the critical parameter for oxygenation of tissues.
The molar concentration of free O$_2$ in plasma is proportional to the partial pressure over the liquid, a fact known as Henry's law. The proportionality constant is the solubility of oxygen in the liquid, about 1.3 10$^{-6}$ M / mmHg for plasma. So at 100mmHg, the plasma O$_2$ concentration is about 130 $\mu$M. For comparison, the O$_2$ concentration in an ideal gas at 100 mmHg is 9 mM, or 70-fold higher.
See for example this book chapter for more information.

By the ideal gas law, PV = nRT, you can find pressure by dividing both sides by volume, P = nRT/V. Since R is a constant, and you can usually assume T isn't changing very quickly for biological systems, you can pretend P = n/V, which is moles per unit volume, analogous to concentration. The reason the units are written in pressure is probably because gases are hard to weigh, but measuring pressure is easy. This also accounts for the affect of temperature, which shouldn't affect the soluble ions you mentioned, but would affect the "concentration" of gases.

No, this is not correct. The ideal gas law is not applicable here, since blood plasma is not a gas! Blood gas (partial) pressure refers to the pressure over a gas in equilibrium with the liquid. To find the concentration in blood, you must take in account O2 solubility in plasma and also the effects of hemoglobin. The actual plasma concentration is much smaller than the concentration P / RT in air. (And also you cannot pretend P = n/V; there is proportionality, but not equality.)

@Roland I don't think OP was looking for a lecture in physical chemistry, but rather why the concentration of dissolved gases are expressed as pressure rather than a molarity. The ideal gas law should be a "close enough" demonstration that pressure is analogous to molarity, especially considering the practical aspects of taking measurements 100+ years ago when these unit conventions were put in place. If OP wanted to know how to determine the affinity of O2 for hemoglobin, that would be different, and the ideal gas law would be insufficient.

Well, solubility is not a minor detail here, the concentration I get from the ideal gas law is 70x higher than the plasma concentration.  And solubility + hemoglobin is the reason why concentrations are given in pressure, I think.  See my answer.


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Do cortical cells in root have higher water potential than endodermal cell solution?Or is it the other way round?
Well, water normally passes from root hair cells to cortex to endodermis, and from there to the xylem vessels. All of this occurs down the water potential gradient by apoplastic or symplastic pathway through these cells. I was wondering how water potential differs in each of these cells for water to be transported. BTW I'm confused why my teacher said that the water potential in xylem vessels(the tracheids) is highest among all the cells I mentioned. Then how come water can move down the water potential gradient?

It's the "higher" when you take only the value, or mathematically speaking the absolute value. Suppose the water potential outside the root is 0 KPa, and inside the tracheid is -10 KPa (I'm making up those numbers). We tend to say that the potential inside the tracheid is higher, but mathematically speaking it's lower. Water will move from exterior (0 KPa) to the tracheid (-10 KPa), going from the higher pressure to the lower pressure, not the other way around.

So the water is moving from less to more negative water potential, but at the end of the day it will be the tracheids which will have most of the water, right?

Don't think about "from less to more negative", it's mathematically confusing. Water moves from higher pressure to lower pressure. If the pressure in a pond is -2 KPa and the pressure in the tracheid is -10 MPa, water will move from the pond to the tracheid (-2 is higher than -10). If the pressure in the leaf spongy mesophyll is -50 MPa, water will move from tracheid to the mesophyll. And if the pressure of the air is -100 MPa, water will move from the mesophyll to the air. In the end, water will move from the pond to the air.

Thank you so much for explaining. It's all clear to me now.

No worries. And just correcting what I wrote: -2 is higher than -10000 is the correct sentence between the parenthesis, because I compared -2KPa with -10000Kpa (-10MPa).


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H is the set of all possible Diplotypes that are consistent with genotype data
I am new to Biology.SX. I have a statistics background, and have almost zero knowledge in genetics. I am trying to understand some things related to genetics in a certain paper of biostatistics.

Haplotype data were simulated using the haplotype patterns and frequencies (shown below) for 5-SNPs along a dabetes susceptibility region on chromosome 22, reported in FUSION study.

I know that haplotypes can be represented as binary sequences. I wonder why all the possible $2^5$ are not present here. (?)
The paper also says that

Let $G=(g_1,\ldots,g_M)$ denote the unphased genotype data for the $M$ loci. $\mathcal{H}_G$ denote the set of all possible diplotypes that are consistent with the genotype data $G$.

If a subject carries at most one copy of the causal haplotype '01100', it belongs to dominant genetic model, if it carries two copies of this haplotype, it belongs to recessive model.

The set $\mathcal{H}_G$ is not clear to me. While computing the likelihood, I need to know $\mathcal{H}_G$. Any help or suggestions?

Disclaimer: Like the OP, I know very little about genetics and I suppose other people in the site can give better answers than me. Anyway, since the question has been unanswered for months I'm posting my answer. Hopefully someone will improve it.
Just beware that "possible" in this context doesn't mean all haplotypes that we can imagine. As the paper says, "$\mathcal{H}_G$ denote the set of all possible diplotypes that are consistent with the genotype data $G$" and that is an additional restriction that allows just some diplotypes - the seven ones listed, not the 32 we can imagine.
Furthermore, please notice that sum of frequencies in the table equals 1, therefore there can be no more haplotypes in the set.
However, it would help if you linked the source where you got those data and quotes.


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Species Identification: Bulbous root on plant, Southern California, USA
In Southern California, I was pulling out some roots and grasses and weeds in our backyard, and I noticed something weird. It appeared like there was a grape-sized bulb of something connected to one of the roots below the top layer of dirt. I didn't puncture it or anything, but do you have any idea what this could be?
It reminded me of two things: an air sack on kelp and a potato.
Edit: I took some more photos, and I tried to break it apart. I was able to break it in half with one hand, easier than a potato but harder than a grape. It was a little juicy inside. I took more photos too.
Edit number two: We have dandelions. Does this seem like it could be a potato dandelion?

Edit #3: So we have a lot of Dandelions and I thought these roots appeared to be connected to dandelion plants, so at first I thought they were potato dandelions. However, we I pulled out a different plant nearby, and it had very similar looking tubers connected to the roots. It was a small plant, but here's the picture, and a picture of a larger plant that I think is the same species as this one, but mixed with a bush. Can anyone positively identify it?

Edit #4: Here's more pictures of the plant I'm seeking to identify, which appears to be a more developed individual on a neighbor's property, and it even has berries:

Does it taste like a potato?

@GrahamChiu Does it look like a potato? I'd rather not taste it or touch it for that matter.

I do believe this is a potato dandelion. An answer that can confirm this would be nice.

I don't think taste is a basic identifying character as well I think its NOT okay  taste random an unidentified species. As a natural trend; many species with tuber-like food-storage organs, accumulate toxic metabolites (and belong herbal medicine, too) perhaps so that predators like mice or insects doesn't eat them up.

This is an Asparagus species, and the root bulbs are storage organs. Unfortunately, I can't identify the species. There are 219 accepted species currently in TPL. I presume this is an ornamental plant. As far as I can see, the species is not recorded as naturalized in California.

Are you sure? Nothing on the plant looks like asparagus. It does appear to have berries on a more developed plant that I saw in the neighborhood.

Actually maybe you're right, I did an image search for a random one of those species on your list, "Asparagus altissimus", and that looked kinda like this and had berries too. Are the berries and tubers and plant all edible do you know?

I am aware that some Asparagus species root bulbs as well as young subterraneanous shoots are famine food in parts of Africa, but I don't know about their any of their properties, i.e. if they contain anything which might be irritating or even poisonous to humans.
[Edit: Young shoots of A. officinalis, of course, are cultivated for human consumption, as you will know.]

Those are root nodules. They grow on root of plants (primarily Fabaceae) . They aren't harmful (but I'm not recommending to eat them). They are natural adaptation that ensures the plant's survival. They are important because they store water too for the plant during periods of drought.

Root Nodule
  this is an asparagus fern. a very invasive plant.

[UPDATE]
About the plant's specie, well, I can't determine. I'm not good at determining plant specie by roots.

@rg255 His question was "... but do you have any idea what this could be?" and I answered that. About identifying the specie (which was mentioned in the title), I can't say from what plant are those "balls" because I can't identify clearly the roots/leaves in the photos. He just said "...I was pulling out some roots and grasses and weeds in our backyard..." But if you do know what kind of plant that is, then feel free to drop an answer or add it and edit my answer.


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Hybrid vs introgression zone in natural populations
In the book An Introduction to Molecular Ecology, the authors say that

Introgression is the diffusion of alleles from one population or
  species into another as a result of interbreeding or hybridization
  between them.

And that hybridization is (roughly) the breeding of two distinct species.
I thought that when we were talking about introgression zone and hybrid zone, it was the same thing.

But here is my interpretation:
See the image below. Across an area, you would have 2 populations of 2 species (A-E). They could interbreed in the middle, this would be called the hybrid zone (in C). But the change of allele (or the transfer of allele) between two populations is not only done by hybridization (B vs C). It can be done by a new hybrid breeding with a non hybrid (backcross, in B). Then, B to D would be the introgression zone.
I don't really know what would happen in that case when 2 hybrids breed together for the colours!
So my question is: What is the difference between introgression zone and hybrid zone (is my interpretation correct?)?

I think you're correct. See Harrison, R.G. and E.L. Larson. 2014. Hybridization, introgression, and the nature of species. J. Hered. 105: 795–809. Also see https://www.differencebetween.com/difference-between-hybridization-and-vs-introgression/
Interesting that you're received no responses to this. It's an interesting (and I think important) question.

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


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How do traits with no negative effects get "weeded out" via evolution?
If only those who are most fit to reproduce are the ones reproducing the most, it makes sense that traits that prevent one from reproducing would eventually disappear from a population.
But what about traits that have no effect on reproduction, like the presence of wisdom teeth? Humans don't need them, but they don't inhibit us from reproducing either. So how do humans evolve past the point of having wisdom teeth or other similar traits with no negative effects?

Maybe in some cases the expression of the trait with no negative effects is linked to one that is, so thereby if the organism is expressing the negative trait it would also express the non negative trait, and then that would be selected against. I am just a layman though, I would wait for a more clear response...

They DON'T. Remi's answer down there is pretty comprehensive, but it really should point out with much more emphasis that non-negative traits can remain in the populations for millions of years, if not forever, unless a random mutation+drift removes it, which is a pretty low chance event.

Following up on the comment by @Davor vestigial organs are an example of useless traits sticking around. Having an appendix won't help your offspring to flourish, but it won't diminish their chances either

Oops I wrote a lot! This is almost a very brief introduction to some concepts of population genetics.
A little bit of terminology first
Locus
A locus (plur. loci) is a position on a chromosome.
Allele
At a specific locus, different individuals may have different variants. One individual might be ATTCTA while another might be ATTCAA for example. These variants are called "allele". The whole goal of evolutionary genetics is to understand the creation (mutation) and change in frequency of the different alleles in the population.
Heterozygosity
You probably know that in many species, we carry two copies of each chromosome. One individual can therefore carry twice the same allele at a given locus or can carry different alleles. Expected heterozygosity ($H$) at a given locus is the fraction of the population that carries two different alleles at this single locus.
Fixation
When an allele reaches a freuqency of 1 (100%), that is only this allele exists in the population (and therefore the other alleles have been wiped out), we say that it has reach fixation.
Natural Selection
The process you describe in your first paragraph is called natural selection.
Natural selection is a fitness (=a function of both reproductive success and survival) difference between different genotypes. As you said (but with other words), deleterious alleles will decrease in frequency through time and will eventually end up being weeded out from the population through natural selection.
Genetic Drift
There are other evolutionary processes than natural selection. Typically, the one we will be interested in to address your question is genetic drift.
What is genetic drift?
Genetic drift refers to the random sampling of a population in order to build up the next generation population. There are different ways to model genetic drift (Wright-Fisher model, Moran model, coalescence model) but without having to talk about the details of these mathematical models, it is important that you can conceive the role of random sampling in the change in allele frequency through time. For this, I invite you to first read Why is the strength of genetic drift inversely proportional to the population size? and when you have finished, come back to this post.
One the below figure, you can see the effect of drift through time. The below graph consider a bi-allelic locus (a locus where 2 and only 2 different alleles exist in the population) starting with an initial frequency of 0.5 (=50%). Each line is a separate simulation and shows the frequency of only one of the two alleles.

The above graph considered a population of size $N=100$ individuals. Below, the same types of simulation with a population size of $N=25$ individuals. As you can see that the genetic drift is stronger

Every single locus is subject to genetic drift whether it is under selection or not. However, if a locus is under strong selection, then genetic drift with have little power to explain what allele will get fixed in comparison to when the locus is neutral.
Genetic drift and loss of alleles
It is clear from the graph above that genetic drift also wipe variant out of the population. We just don't know for sure which variant will be wiped out. To be more accurate, the expected heterozygosity due to genetic drift is reduced by a factor $\frac{1}{2N}$ each generation. One can make plenty of calculations from basic models of genetic drift. For example the expected time to being wiped out is $\bar t(p_0)=-4N\left(\frac{p_0}{1-p_0}\right)\ln(p_0)$, where $p_0$ is the starting frequency of the allele of interest.
A interesting result is that the probability of an allele to reach fixation is equal to its frequency. If there are $N$ individuals in the populations, there are $2N$ alleles (but not $2N$ different alleles). If there are, say 235 alleles A in the population and $2n - 235$ alleles B in the population, then over the long run (so that one will necessarily fix) the probability of fixation of the allele A is $\frac{235}{2N}$ and the probability of fixation of the allele B is $\frac{2N-235}{2N}=1-\frac{235}{2N}$.
Wisdom teeth
In your question, you are interested about a supposedly purely neutral locus. You talked about wisdom teeth I suspect more as an example rather than because you are interested to this trait.
Let's assume that the presence of wisdom teeth is completely neutral. Note by the way that as a rule of thumb if $2 N s << 1$, (where $s$ is the selection coefficient on a given allele) then the allele will behave essentially as if it was a neutral allele. So, if wisdom teeth is neutral, then the probability of this trait to disappear over the long run depends on the frequency of the allele causing this trait. So far, I have assumed that we were interested in a single locus only. In reality, variation in many traits are caused by variation at several loci. In such case calculations are a little less straight forward (but still feasible). I do not know the genetic basis of wisdom teeth, so I cannot make good predictions for the evolution of this particular trait.
Other evolutionary processes
Here are a few example of interest
Gene flow
Note of course that there are other processes to consider when trying to predict the fate of a given allele or trait. For example, in a given population you might have a flux of migrants that come from a population where one allele is fixed therefore affecting the allele freuqency in the focal population. This is called Gene flow.
Hill-Robertson effects
Never forget that a locus is not alone on its chromosome. It is physically linked to other loci and selective pressures at other loci will affect the allele frequency at the focal locus. This is called Hill-Robertson effects.
Mutations
Of course, when a locus is not polymorphic (has only one allele), mutations is the ultime source of variation. When a locus is polymorphic, then it is likely the mutations will have a minor effect on the allele frequency (although it depends on the size and type of locus and depends on whether mutations can make up new functional alleles).
Pleiotropy and covariance between phenotypic traits
Phenotypic trait do not evolve independently. If wisdom teeth is a consequence of the activation of the molecular pathway for resistance to HIV (which it very probably is not), then wisdom teeth will not evolve as a neutral trait. A locus that affects several traits is said to have pleiotropic effects.

You are correct in thinking that traits that improve (impede) ones reproductive rate should be spread through (removed from) the population by selection. However, the process of evolution rests upon more than just selection.
There are four mechanisms by which evolution operates; mutation, migration, drift, and selection. Mutation brings new variation in to populations, with changes occurring in the DNA (e.g. an A becomes a T in the genetic sequence). Migration can both add and remove variation from populations, but is a within species mechanism of evolution (by definition there should be no genetic migration between species). Drift is the change in genetic variation that comes from random variation in reproductive success. With drift there is no link between the genes and the rate of reproduction, i.e. carriers of one allele are equally likely to reproduce equally well as carriers of alternative alleles.
Selection operates when there is covariance between reproduction (fitness) and the genes one carries, i.e. there is a tendency for the carriers of one allele to produce more offspring than the carriers of an alternative allele. This might arise because, for example, the gene improves fertility.
When you are considering the evolution of neutral (or nearly neutral) traits you are considering evolution via the first three mechanisms (mutation, migration, drift). Small populations are prone to losing genetic variation by drift more so than large ones, here is a simulation of 10 populations over 250 generations, where the population size is 200 on the left, and 2000 on the right. You can see that the smaller populations have a higher tendency for fixation of one allele, this is with no selection occurring.
Many neutral traits persist for many generations because it is just a lottery, eventually they should be lost from the population, but we can't tell when.

Furthermore, the genes that cause neutral variation may be under no direct selection, but could be in linkage with loci under selection, thus be affected by indirect selection, or they could have multiple effects (pleiotropy; e.g. the gene causing the expression of a neutral trait also affects the expression of a selected trait).


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How is oxytocin produced?
Is oxytocin (or other peptide hormones) produced from a gene through translation, or is it made some other way?

seems like a straightforward question...all proteins are translated from mRNA that is transcribed from DNA - that's the central dogma of molecular biology - is there a reason you think that it could be made another way?

Peptides like oxytocin (I think it is only 9 AAs long) seem small enough that maybe a cell would synthesize them using proteins rather than by a ribosome translating a gene for them.

Some peptides are synthesized via nonribosomal peptide synthetases, so the question seems legit.

Oxytocin is produced by cleavage of the protein of the oxytocin/neurophysin I prepropeptide gene. The precursor peptide is cleaved by Proprotein-Convertase 1
. Mice lacking the gene which encodes for this enzyme have reduced levels of oxytocin. The final step in the biosynthesis of oxytocin is carried out by Peptidyl glycine alpha-amidating mono-oxygenase.