text:
What could explain discrepancies between dates provided by the fossil record vs. the molecular clock?
I am studying a mud snail genus called Ecrobia. For the Caspian species (Ecrobia grimmi), there is a discrepancy between dates provided by the fossil record and the molecular clock:

First appearance of Ecrobia grimmi in the fossil record: Middle and Upper Miocene (15.97 to 5.33 million years ago)
Age of Ecrobia grimmi as suggested by the molecular clock: 0.58 to 2.04 million years. The molecular clock was calibrated using an external marker-specific clock rate, and the climax of a geological event.

What could explain this discrepancy?

Could you give the sources for both dates? It would make finding the answer easier because afaik there are many different things that could account for discrepancies between molecular clock dates and fossil dates. For one thing, what was the molecular clock measuring exactly? Divergence from closest relative, and if so what relative was it? Age of common ancestor of extant individuals?

As @Oosaka said, there are many reasons that molecular dates can be discordant with fossil dates. Without actually knowing what methods you've used to generate the molecular date, we can't be much help. For example, it could be due to lineage-specific rate heterogeneity, if you have used a method which assumes a strict clock.

The source for the fossil record is Asnafi 2010, the source for the molecular clock is my own ongoing study.
The molecular clock was measuring the divergence from closest relatives; all Ecrobia spp. were included.
The age of the common ancestor is ca. 15 Ma.
The molecular-clock analyses were run with *BEAST.
The results of the strict- and relaxed-clock analyses were similar.

First, the example you give is unusual in that molecular dating analysis should be calibrated with fossils to set minimum ages. If Ecrobia grimmi exists in the fossil record, then no proper molecular analysis would estimate them to be younger than those fossils. There are two main causes of discrepancies between fossil and molecular dating.
For fossils you never find the oldest example of a species. If a species diverged 100 million years ago, you might not find a fossil of that lineage for millions of years, meaning that fossil estimates are almost always underestimates, but they do form a baseline upon which to calibrate molecular data. The problem with molecular data is that there is no "molecular clock". Lineages, genes and individual nucleotides all change at different rates. The best you can do is plug in fossil and/or geological dates into a model that is based on other lineages. Hopefully you have calibrated dates for closely related species, and the same genes. Even then, you do not know that the lineage you are working with will follow the same rates as the model predicts. At a minimum, you need to set a minimum possible age in BEAST to 5-16 mya.

I cannot use fossils to calibrate the molecular clock because Ecrobia spp. are cryptic (i.e. they are morphologically indistinguishable). Therefore, I thought the discrepancies between fossil and molecular dating might be due to a misidentification of the fossils: fossils identified as Ecrobia grimmi could actually be of a different Ecrobia sp., or alternatively, of an ancestral species. What do you think about that?

Fossils are the gold standard. But if you cannot trust their identity, then you were right to exclude them. But without a reliable calibration, I don't think molecular dating is worth doing at all. Better to not know at all than to "know" something that is wrong.

What do you think about using external marker-specific clock rate and/or geological events to calibrate the molecular clock?

@JustineVandendorpe I think they are OK, but need to be pretty solid. For example, the formation of the isthmus of Panama is well established. Is Ecrobia marine or freshwater?

Ecrobia is a brackish genus (from 6‰ to 38‰).


text:
Choosing PCR conditions
How does one choose PCR conditions? Does it depend on the taxon, on the DNA concentration, on the primers or anything else?

You need to first build an initial protocol and then optimize it.
The most important to determine the conditions is the polymerase used. Some polymerases work at higher or lower temperatures and will work faster or slower. Find the default protocol from the polymerase seller and this will give you a good idea where to start.
The second most important is the primers used. Depending on the GC % in the primers and their length, the times or temperature of each step will change, or if you prefer will need to be Optimized.
The length of the DNA fragments will also determine the length of the cycles. Most polymerase sellers will includes steps to optimize the reaction depending on the quantity of DNA used, primer length and other parameters.
For more information:
Designing primers:
Taq DNA polymerase protocol example:
Optimizing PCR

PCR thermal profile, Deoxynucleoside Triphosphates and Primers are interesting paragraphs

Use primer3 to design your primers, then just use whatever protocol your lab usually used for PCR.
A high annealing temp solves many problems, and a good enough taq won't mind.
I successfully sanger sequenced thousands and thousands of mammalian exons, with primer3 designed primers, a HotStar Taq, and a 60 degree annealing temp.  Worked almost every time.
Obviously if you are doing long PCR, or working with a very high GC or low GC species, that might requires more optimizing.

According to my knowledge the main thing in annealing temperature in PCR
Primers annealing temperature should be selected by keeping in 5° less than the lower melting temperature of primers
Secondly MgCl2 working Concentration also plays a major role in PCR optimization

As you are probably aware there's a lot more to designing a PCR, as the previous answers have suggested.

source: Stack Exchange

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

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

sort: votes


text:
Performing PCR on samples whose DNA concentration is nul
Is it vain to perform a PCR on samples whose DNA concentration was measured as nul by a NanoDrop?

Nope, you could get amplification from samples that are orders of magnitude below the nanodrop detection limit (~2 ng/uL). To compare: most manuals for polymerases recommend 1 ng of plasmid template, and will probably work with much less, especially if you use a few more cycles.
But if you expected to see something on the nanodrop, and you get nothing, something else might be completely wrong.

You can go down into the picogram range. And you could use nested PCR to ensure specificity.

Some times nanodrop is unreliable. However, to be sure that you are not wasting your time, I would redo the extraction. Nanodrop in a lot of PCR methods is a control test to validate that the extraction went well. So, I would redo the extraction if I where you.

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


text:
How to design internal primers?
I have sequences of the Cytochrome c oxidase I (COI) from several populations of Peringia ulvae (Mollusca; Gastropoda; Littorinimorpha; Hydrobiidae). I need additional COI sequences from a specific population. When using the same primers and PCR protocol as for the other populations, I do not get any PCR product for the specific population. My PI suggested me to design internal COI primers for Peringia ulvae. How can I do that? Should I use the COI sequences from the other populations?

You could try simply ordering a degenerate version of the primers you have. If possible, try aligning the sequences for many known COI alleles from your organism and see which bases in particular are variant. If the sequence is conserved, keep that base, if it is variable, add a degenerate/random nucleotide in to your primer order. The mix of primers you get back will then have every possible variant for a given position, and that might help you to get amplification.

Try to lower the annealing temperature of your PCR. If there are few mismatches between the DNA sequences of the different populations you may be able to amplify them all with the same primer set by making your annealing less stringent. One question, are the primer annealing inside the coding sequence of COI or on the flanking region?

@alec_djinn How can I know where the primers are annealing?

@JustineVandendorpe do you know the sequence of the primers? If so, then just use BLAST to understand where they anneal.

@alec_djinn I know the sequences and ran a BLAST. Thanks a lot!

If you are not getting amplification, there are multiple things to visit before you want to design internal primers. You should try troubleshooting your PCR reactions before designing and ordering internal primers. If you are doing the PCRs wrong, it is likely you will run into the same problems again with internal primers.
There are excellent guides to trouble shooting PCRs - Just a google search "Trouble-shooting PCRs" should give you a lot of material to go through. This is from NEB, but there are several others, each manufacturer having their own, so you could refer to one of whose reagents you are using.
Primers generally give good reads from the 5' end for about 600-700 bp and after that the quality of base calling deteriorates, so if your target amplicon is above 1500bp or so, you would need internal primers because the 'external' primers would give you good sequences for only 1400 bp or so (600-700 bp from both directions, for fwd and rev primers). So internal primers can be used to sequence the regions that cannot be reached by the main (external) forward and reverse primers. The published papers from where you are using the external primers will most likely have the internal primers if CO1 is long enough to require internal primers.
Otherwise, you would need to align the existing sequences from the other populations, and look through regions of the alignment that are conserved which could act as potential priming sites. There are other issues to be taken care of before you can consider a 'conserved region' a 'priming site' and go ahead and order primers. Again there are excellent primer design tutorials available, just a google search away.
Let me know if any parts of the answer are not clear, or sound like jargon and I will do my best to simplify it for you. However, I would strongly suggest troubleshooting the PCR first - for e.g. trying a gradient PCR to find the optimal annealing temperature.

Thank you very much for your answer. I am also using the reagents from NEB so I had a look at their Tm Calculator. With the parameters I entered, I got a warning message saying: "Tm difference is greater than the recommended limit of 5 °C." Do you know how can I solve that?

Hi, what is the annealing temperature that you are using in your PCR and what is the Tm for your primers?
Also, do you have something like Nanodrop readings of your DNA samples? Do you know their concentration? If the concentrations are too high/too low, PCRs will be inhibited.

I am using an annealing temperature of 52 °C. The Tm suggested for my forward and reverse primers are 49 °C and 59 °C, respectively. The DNA concentration of my samples ranges from 0 to 870 ng/µl.

870 is WAY too high. Generally 25-100ng of DNA is recommended in the reaction mixture.


text:
How can you develop a bacterial infection when taking antibiotics for another area of the body with a bacterial infection?
How can you develop a bacterial infection when taking antibiotics for another area?
For example, "if someone was prescribed an antibiotic for a bacterial infection of the throat and while taking the antibiotic tablets they developed a bacterial infection in their toe.  Explain why the antibiotics taken for the throat did not prevent the growth of the bacteria in the toe".
Is it because the bacteria in the toe is a different type and didn't respond to the bacteria developing the toe (don't think so, but not sure), or
was It because antibiotics don't prevent the development of bacteria they only inhibit it once grown and kill it, or
something else?

More information would be needed to answer this properly, but it sounds like you've got it. The antibiotics for the throat infection would be present in the toe, so one should conclude that those antibiotics are ineffective against  the bacteria causing the new toe infection. If this is homework, please add the homework tag, whereas if this is a personal medical question, I'm afraid it's off-topic.

Your first assumption is mostly correct

Bacteria in the toe is a different type and didn't respond to the
  [antibiotic taken for the throat infection].

the reason being because it outlines some essential characteristics of "antibiotics" and antimicrobial drugs in general.
Selective Toxicity and Mode of Action
A very important characteristic of an antibiotic is its selective toxicity. An ideal antibiotic has a high level of selective toxicity meaning that it will only target the bacteria that is causing an infection while not damaging the host tissue (cells) and the person's biota (resident microorganisms). This characteristic generalizes antibiotics into two categories; broad-spectrum (low selectiveness) and narrow-spectrum (high selectiveness). For example, a broad-spectrum antibiotic will target both gram-positive and gram-negative bacteria while a narrow-spectrum antibiotic will either target gram-positive or gram-negative not both.
Another characteristic of an antibiotic is its mode of action or in other words the area of a bacterium that it targets to inhibit/kill it. Most commonly antibiotics target one or more of the following areas/processes:

Cell wall synthesis,
Cell membrane function,
Protein synthesis, and
Nucleic acid synthesis

It is important to know this because mode of action goes hand in hand with selective toxicity, for example an antibiotic that targets membrane function might prove ineffective against bacteria that form capsules another themselves.
So to answer your question

why [did] the antibiotics taken for the throat not prevent the growth of
  the bacteria in the toe?

We can reason that the selective toxicity of the antibiotic taken for the throat was narrow or that its mode of action only targets the bacteria causing the throat infection but not the bacteria causing the toe infection.

Thanks that's exactly what I needed! Thank you for that I understand now :)


text:
Cyanobacteria: Gram negative or Gram positive?
My (school) textbook states that cyanobacteria ("blue-green algae") are Gram positive (no references provided). They mention this at several points over the chapter we're doing so it doesn't look like a typo.
However, this Wikipedia article on "Gram staining" (under "Gram negative bacteria") states:

Gram-negative bacteria generally possess a thin layer of peptidoglycan between two membranes (diderms). Most bacterial phyla are gram-negative, including the cyanobacteria, spirochaetes, and green sulfur bacteria, and most Proteobacteria (exceptions being some members of the Rickettsiales and the insect-endosymbionts of the Enterobacteriales).
 Emphasis, mine.

There is no mention of cyanobacteria under the section "Gram positive bacteria".

I understand that there is a possibility that some cyanobacteria stain positive, and other stain negative (owing to the lack of a very sharp definition for "cyanobacteria", as well as the limitations of Gram-staining).
So what I want to know:
1) Are cyanobacteria generally Gram positive or Gram negative?
2) Are there exceptions to that general trend? If so, what are they?


text:
Are centrioles really absent in human neurons?
A booklet (issued by my school) claims,

Centrioles, formerly believed to be absent in neurons, have been described in neurons and may be associated with the production and maintenance of neuro(micro)tubules in them.

I was under the impression that mature human neurons are totally devoid of centrioles.
Being something circulated at a school, it lacks niceties such as citations/references. I've done a spot of Googling, but that didn't yield anything confirming the claim in the booklet.

Q- As per latest studies/info. do (mature) human neurons really possess centrioles?


text:
Stem cell and organ growing genitals
I've been reading a lot about stem cell research and the work on growing artificial organs.
I assume, with sufficient advance in the technology, there is no theoretical reason it would not be possible to grow genital organs (gonads, uterus) in particular?
So my question is: is there any theoretical reason you could not use this process to grow the genital organs of the opposite sex of a stem cell donor?
So then, would an ovary grown from male stem cells potentially ovulate Y-gamete eggs?

No one knows if a uterus is capable of producing so-called "Y-eggs", because in persons affected by sex chromosome abnormalities (XXX and more, XXY, X, XYY, etc.), the presence of a functional Y generally produces a male phenotype, whether or not they are sterile or have natural levels of testosterone, because the Y contains the sex-determining gene SRY and other male developmental and fertility factors. In contrast, people with only X chromosomes (regardless of the number) are generally female-appearing, with at least some development of the associated organs and structures.
A second question is whether a male-derived stem cell could be coaxed, hormonally and otherwise, to become a uterus in the first place. An X is already present, so all the purely genetic (though not necessarily epigenetic) instructions are there, but, as far as I know, the question of whether a Y would interfere with the development process has not been answered in humans.

For some reason I'm having a difficult time finding information on persons with only a Y chromosome. Going back to my undergraduate days (boy, was that a long time ago), I seem to recall that they're likely non-viable, but I can't find anything now to back that up.

From what you say, it sounds like it would be even more of a stretch to create testicles from a woman's stem cells.

@StephenPosey correct, as women lack the necessary Y chromosome.

"the presence of a functional Y generally produces a male phenotype, whether or not they are sterile or have natural levels of testosterone, because the Y contains the sex-determining gen" : Did you consider chimerism arising from "vanishing twin syndrome" & the like, the guest cell lines arising from this most often take their cues from their host organism, so a male vanished twins cells can persist in a female sibling but should in no way result in a male phenotype

^ further, were the larger portion of one of these colonies of cells from a male sibling to be in the ovaries of a female host there is absolutely no reason to suppose that (having "gone native" & taking all of their cues from the host body on what they're supposed to become & do) they wouldn't produce perfectly normal egg cells, half of which could be expected to carry a Y chromosome.

^ though as the ovaries are internal the chances of any loose cells sloughed off from a twin in the womb being absorbed into the area slated to become the ovaries seems slim at best, the other way around though, a sample of a female twins cells colonizing the external location of a male sibling in the womb where the gonads are slated to form, doesn't seem that unlikely.


text:
Protein-protein interactions search
I used STRING db in order to find all the interactions of the precursor protein APP. What I specifically need is a confirmation (supported by some article and experiments in it). But significant amount of interactors have only "Database" confirmation (mostly relaying on Reactome and KEGG data). Searching in these db's gives me neither article nor even the presence of these proteins in one pathway (what's weird). How can I obtain the data?
Thanks in advance!

Could you add the specific KEGG identifier?

@James As an example for some protein?

There are several reasons why you might not be able to find the references. You might not know what you're looking for or perhaps the specific protein is unreferenced. It would be useful to start with your example and work from there.

You can try to use IntAct Molecular Interaction Database. The data in this database is based on:

data from the literature or from direct data depositions by expert
curators
<300k binary interactions in 2011  developed by the EBI's
Proteomics Services Team
recent reference: Aranda et al. '10

This is also mentioned in the summary of the Aranda et al.'10 article:

IntAct is an open-source, open data molecular interaction database and
  toolkit. Data is abstracted from the literature or from direct data
  depositions by expert curators following a deep annotation model
  providing a high level of detail. As of September 2009, IntAct
  contains over 200.000 curated binary interaction evidences. In
  response to the growing data volume and user requests, IntAct now
  provides a two-tiered view of the interaction data. The search
  interface allows the user to iteratively develop complex queries,
  exploiting the detailed annotation with hierarchical controlled
  vocabularies. Results are provided at any stage in a simplified,
  tabular view. Specialized views then allows 'zooming in' on the full
  annotation of interactions, interactors and their properties. IntAct
  source code and data are freely available

Further you can use the Evidence tab in String(I assume you have already tried this but in the case you did not):

You can then click on Experiments, then something like this will show up:

You can see how (e.g. Reconstituted Complex assay) and you can see from which article this interaction is coming from if you click on an item in the table:

STRING database shows the protein-protein interaction network and scores according to the presence and absence of experimental verification which can be protease assay, bait coimmunoprecipitation, western assay etc.
if you need further confirmation you should read as much as related articles as possible related to APP.


text:
Can somebody be deaf to voices of some people only?
The voice of females is generally of high frequency, while that of males is generally of low frequency.
Also, as we age, we gradually keep losing the ability of hearing sounds of high frequencies.
So, can such a situation occur when a person is not able to hear voices of females, or maybe of certain people, while he can hear the voices of other people? I tried searching about it, but found nothing.

I think it's unlikely, while female voices may be relatively higher in frequency than male voices, I think the frequencies lost with age are much higher

I can confirm that the wife's voice demands far less attention from me than do the childrens' voices. That said, she would argue that I give her far less attention that I do the the children...

Although you loose the high frequencies in your hearing with age (20kHz and below), this is highly unlikely. The frequency spectrum of our voice is pretty much limited, which is also shown by the fact the for normal telephone, the spectrum transmitted is located between 300 and 3400Hz and the spectrum band between 300 and 3000Hz is named the "voice band". See here for some details.
According to reference 1 the "voice fundamental frequency" for men is between 85 and 180Hz (depending on the reference) and for women between 165 and 255Hz. These frequencies are close enough together to rule out specific hearing of male or female voices. Furthermore the frequencies even overlap.
What happens in age-related pathological hearing loss (also termed Presbycusis) is that voices generally get muffled due to losses in the spectrum and hearing intensity. See the Wikipedia link and also reference 2 for more details.
Reference:

The frequency range of the voice fundamental in the speech of  male
and female adults
Presbycusis

Sensorineural Hearing Loss (SNHL) can reduce the ability to hear faint sounds even when the sounds are clear and audible. Tone deafness in contrast affects a person's ability to learn music, but not the ability to perceive or recognize speech.


text:
What are some examples of small-scale physical phenomena that snakes fear?
What are some ways to use technology to repel snakes?
One idea I was researching is low-frequency sound, which I read snakes could "feel" even though they are naturally deaf. Would this be a viable option? What sound ranges would need to be used?
What are some other ways? Could targeted light be another option?


text:
how to calculate dilution factor and CFU
I'm very confused
I did a bacterial experiment where i added 5 grams to 70ml of distilled water that contains 10g of fresh meat. I left it in a sampler container over 24 hours then i cultured bacteria from the broth using an incubating loop onto nutrient agar. I left them to culture then observed 29 colonies of bacteria.
I observed 1 bacterial colony under a light microscope and counted 19 bacterias.
How do i calculate the dilution factor and CFU?
i need to calculate how many bacterias were on the agar plate?
please help!

Do you know what CFU stands for?

What are your workings out so far? Did you record what magnification you viewed the colonies under? ( Eg. 200x ). Did you use a hemocytometer?   If you did, Google hemocytometer and lots of info will come up about finding the number of CFU including the formula/s required.


text:
I can't see anything at all in my microscope
I just got the Amscope M102C microscope, and it is the first microscope I've operated. I decided to try to look at a fly leg at 40x magnification, but all I could see were the blobs in your eye you get from looking at something bright, as well as a few dots that appear to be on the lens. I tried focusing, cleaning (even though it was fresh out of its package), but I still couldn't see anything. It's so blurry I can't even make out any shapes. Could I please have some help?

40X is almost certainly an immersion objective, this type of objective isn't meant for looking at things like fly legs, it is meant for looking at tissues and cells. You are probably looking for a dissecting microscope. Hopefully your microscope came with some instructions.

Any 40X objective I've used is not an immersion lens. Furthermore, 40X magnification implies 4X objective and 10X ocular. But, yes, a dissecting microscope should be used for this application. Compound microscopes are not ideal for looking at thick, 3D objects.

Understood, but I've also observed (or tried to) onion skin, blades of grass, and a strand of hair and there would be no way of telling there was even anything under the microscope at all.

There are YouTube videos that will take you step-by-step through the process.

@canadianer Right you are - when I read the post at first I read it as the 40x objective rather than the full magnification. My mistake.


text:
Why doesn't the sperm die if there is citric acid and acid phosphatases in the semen?
While studying I read that sperm needs alkaline medium for its survival.But when I studied the composition of semen it revealed that semen contains citric acid which acts as a sperm nutrient along with fructose.It also contain acid phosphatases.So in such sitution how can the sperm survive?

Can you provide some sources?

From TextBook of Medical Physiology By Guyton and Hall.

Citric acid is a weak acid so in the context of a buffered physiological medium (semen pH 7.7) it will not cause any significant acidification. Acid phosphatases are enzymes with a pH optimum below 7 (as distinct from alkaline pho sphatases). Their presence has no implications for the pH of semen, although it is interesting to speculate why an alkaline fluid would contain an acid phosphatase.

Vaginal pH is ~4. The acid phosphatases likely have some function in this environment.


text:
Are cell lines potentially dangerous?
More specifically, if a human subject was exposed to, say, a human cancerous cell line (via intravenous injection or through an open wound, for example), is it possible that they would develop any conditions associated with the cell line?

This post will probably interest you.

This is highly unlikely because the immune system would detect these cells and atack them as foreign. There is at least one case described in the literature in which a woman died of lung cancer after receiving a donor organ from a smoker. This is due to the fact that after transplantations people have to take drugs to suppress their immune system to avoid an immune reaction against the transplanted organ. This allows tumor cells to survive.
The same problem is true in research animals. For the transplantation of tumor cells you need mice with a severely deficient immune system (so called "SCID" (Severe Combined Immunodeficiency) mice) to allow tumor cells to grow. This is different when you work with viruses (like the human papilloma virus) which can cause cancer. Here you have to take appropriate safety measures.

This is largely correct, but there much more known cases, including one case of transmission from a patient to surgeon

Thanks for the addition. The case of the Tasmanian devil is also interesting, but these animals are genetically so closely related that the immune system is not detecting the foreign cells as not own.

@har-wradim.  Your reference includes specific examples of needlestick transmission in humans-would be useful if you expand your comment into an answer.

No, I don't mean the contagious cancers of devils and dogs. I mean the section, which starts with "Direct transmissions of cancers are not entirely restricted to animals..."

I read this as well. And it says that this is very rare and from the cases cited only one (the one of the surgeon) is from a person without an affected immune system. As I said: It is highly unlikely...

@Chris. (The needlestick with the cell line was also not immune compromised).  I'm not sure these reports  can say much about likelihood of growth after a puncture, other than the frequency of suitable puncture incidents is probably very low.  Imho, if anything, these reports remind us that there's probably plenty of room for improvement in our understanding of the immune response.


text:
Did the eugenics program in Nazi Germany have a measurable effect?
Did the killing or sterilisation of people considered as living a "life unworthy of life" in Nazi Germany have any measurable effect on the "average health" of Germany? Is there any statistical evidence that the rate of (a specific) mental or physical illness is lower in Germany compared to other countries that were not affected by the Nazis  (I guess you would need to have data on the rate of that illness from before the eugenics program as well)?
P.S. Please note, I'm neither interested in discussing the ethics of eugenics, nor in condoning what has happened in its name under the Nazis. I just want to know what the result on average health (if there is such a thing) was.

I think there is no possibility to study this, because there were several other factors having a big impact on the population, for example a war.

I would say that the war had a much greater impact on the population.

As already said in the other comments, the war (and many other factors) is a very important confounding effect and therefore measuring a change in health before and after the sterilization program would not mean that it is caused by the sterilization program. Beside this statistical issue: How do you think that this sterilization would affect health today?

Do you think of reduction in the number of reproducing individuals, yielding to a decrease in mean heterozygosity and therefore causing deleterious recessive alleles to be more often expressed? We could make some calculations to know what is the expected reduction in average heterozygosity. Or did you think about something else? Mental health? Partial recovery of sterility that, for some reason, causes poor gamete quality?

I really doubt that any effect would be visible in a single generation. We'd need data to back that up but I would be surprised if any difference is observable.

I don't see how this answers anything.

As most of the comment have pointed it out, It's nearly impossible to find out. This is my try:
Dr. L Alexander wrote in his paper, Medical Science under Dictatorship:

Hitler issued the first direct order for euthanasia in Germany on
  September 1, 1939, as his Panzers moved on the Blitzkrieg of Poland.
  Organizations with humanitarian-sounding names were immediately set up
  to execute "health" programs, again, under deceptively, euphemistic
  terms. For example, questionnaires collected by a "Realm's Work
  Committee of Institutions for Cure and Care" gathered and reported
  information on patients who had been ill five years or more and who
  were unable to work. "On the basis of name, race, marital status,
  nationality, next of kin, whether regularly visited and by whom, who
  bore financial responsibility, and so forth," decisions were made at
  key universities about which patients should be killed by
  psychiatrists who had themselves never seen the patients.Likewise, the
  "Realm's Committee for Scientific Approach to Severe Illness Due to Heredity and Constitution" was exclusively devoted to the killing of
  children with congenital anomalies or chronic illnesses. In all,
  275,000 people were put to death in these killing centers before the
  Nazi Holocaust.

Law for the Prevention of Offspring with Hereditary Diseases (July 14, 1933)

Anyone suffering from a hereditary disease can be sterilized by a
  surgical operation if, according to the experience of medical science,
  there is a high probability that his offspring will suffer from
  serious physical or mental defects of a hereditary nature.    Anyone
  suffering from any of the following diseases is considered
  hereditarily diseased   under this law:
1. Congenital mental deficiency,
2. Schizophrenia,
3. Manic-depression,
4. Hereditary epilepsy,
5. Hereditary St. Vitus’ Dance (Huntington’s Chorea),
6. Hereditary blindness,
7. Hereditary deafness,
8. Serious hereditary physical deformity.
Furthermore, anyone suffering from chronic alcoholism can be sterilized.

If anyone is trying to get the statistical evidence that Eugenics have even remotely successful, have look at this table:

Current Top 50 death causes of Germany. (Rate = $\frac{death}{1000}$)

They have started various ways to brainwash people, one of them was movies.
$\text{Ich klage an}$

(source: filmportal.de)
Plot: A woman suffering from multiple sclerosis pleads with doctors to kill her
Current Scenario: Germany Rank $18^{th}$ in the world in death due to Multiple sclerosis
Source:

Alexander L. Medical science under dictatorship. N Engl J Med 1949;July 14.
http://www.life.org.nz/euthanasia/abouteuthanasia/history-euthanasia6
Table: WHO, World Bank, UNESCO, CIA and individual country databases for global health and causes of death.

Good answer - I think its worth emphasizing that eugenics is not genetics and the traits that were used were often ridiculous.   For instance race as a primary selector in a genetics experiment is useless - we know that variations within race are relatively large.  Also these traits are terribly complex - eliminating heart attacks or schitzophrenia by eliminating people when they show signs will not do anything if they already have offspring.

@shigeta: I agree. But, What they did was nothing to do with biology, it was politics.

-1? Any reason?

not from me... the site reviewers do tend to be a little technocratic.  the answer could get back to the genetics of what they tried imho, but you can't do everything.  connecting to culture doesn't fly with some community members.  not my opinion, but i've been downvoted for cultural references myself.


text:
DNA extraction for LAMP assay
I am trying to set up a LAMP assay (Loop-mediated isothermal amplification) for the detection of E.coli.
I was told that EDTA can chelate the Mg in my reaction and thus prevent the assay from working (similarly to PCR). Therefore, I hesitate to use TE buffer. Can I prepare my primer mix and extract DNA (using the boiling method) in DNAase free water?
will that affect the quality of my DNA and primers during storage?
Thanks a lot!
Alex

Although this is theoretical a problem, in fact it isn't one. Lets do the calculation around it. EDTA complexes equimolar amounts of bivalent cations (e.g. Magnesium), so 1mM EDTA will complex 1mM Magnesium ions. Lets assume that the PCR reaction contains 2mM Magnesium.
A typical PCR reaction I do has a total volume of 25ul and contains 1ul DNA template in TE buffer (10mM Tris, 1mM EDTA). The final reaction contains 1/25th mM (or 0,04mM or 40nM) EDTA which can complex 0,04mM Magnesium. So instead of running the reaction with 2mM Magnesium, you do it with 1,96mM, which will not be noticable.
Additionally other errors in setting up (pipettes not accurately calibrated, not setting small amounts into the liquid etc.) easily add up to 5-10% error in total, which has a much higher impact in the Magnesium concentration of the reaction than the EDTA. If you use much higher template concentrations (which is usually not necessary), then you can correct for this, but normally this is not necessary.

The conventional Eiken LAMP formulation has an excess of Mg2+.  5 µl of TE with EDTA at 1 mM going into a 25 µl reaction will have minimal impact.  In any case the LAMP formulation can be up adjusted in Mg2+ to compensate, but I doubt this is even necessary.  Besides, bugs will lyse better in the boiling method with EDTA present and it will hinder nucleases.


text:
What are the basic skills required to pursue future studies in theoretical ecology?
I am a student and just about to choose a project for my Master's thesis in biology. I want to pursue studies in theoretical ecology in the future. Between field ecology and computational biology (as my two possible choices) what would be the best option to go for? Suggestions are needed as soon as possible .

I'm voting to close this question as off-topic

Theoretical ecology
From wikipedia

Theoretical ecology is the scientific discipline devoted to the study of ecological systems using theoretical methods such as simple conceptual models, mathematical models, computational simulations, and advanced data analysis. Effective models improve understanding of the natural world by revealing how the dynamics of species populations are often based on fundamental biological conditions and processes. Further, the field aims to unify a diverse range of empirical observations by assuming that common, mechanistic processes generate observable phenomena across species and ecological environments. Based on biologically realistic assumptions, theoretical ecologists are able to uncover novel, non-intuitive insights about natural processes. Theoretical results are often verified by empirical and observational studies, revealing the power of theoretical methods in both predicting and understanding the noisy, diverse biological world.
The field is broad and includes foundations in applied mathematics, computer science, biology, statistical physics, genetics, chemistry, evolution, and conservation biology. Theoretical ecology aims to explain a diverse range of phenomena in the life sciences, such as population growth and dynamics, fisheries, competition, evolutionary theory, epidemiology, animal behavior and group dynamics, food webs, ecosystems, spatial ecology, and the effects of climate change.
Theoretical ecology has further benefited from the advent of fast computing power, allowing the analysis and visualization of large-scale computational simulations of ecological phenomena. Importantly, these modern tools provide quantitative predictions about the effects of human induced environmental change on a diverse variety of ecological phenomena, such as: species invasions, climate change, the effect of fishing and hunting on food network stability, and the global carbon cycle.

Computational Biology
from wikipedia

Computational biology involves the development and application of data-analytical and theoretical methods, mathematical modeling and computational simulation techniques to the study of biological, behavioral, and social systems.1 The field is broadly defined and includes foundations in computer science, applied mathematics, animation, statistics, biochemistry, chemistry, biophysics, molecular biology, genetics, genomics, ecology, evolution, anatomy, neuroscience, and visualization.2
Computational biology is different from biological computation, which is a subfield of computer science and computer engineering using bioengineering and biology to build computers, but is similar to bioinformatics, which is an interdisciplinary science using computers to store and process biological data.

Field Ecology
Ecology can be studied empirically through data analysis, through lab experiments or through field observations and experimentations. Field ecology refers to this last point that is, it refers to empirical ecology in the field.
Conclusion
Potential Misunderstanding
In your post, you seem to suggest that field ecology is a subfield of theoretical ecology. It is not! Either you work as a theoretician or as an empiricist (and then eventually as a field ecologist). Of course many people do both theory and empiric work.
Note that whether you are theoretical or an empiricist working in ecology, you will need to have a good understanding of the theory behind the science of ecology.
Computational biology vs theoretical ecology
In opposition to empirical ecology and field ecology, computational biology and theoretical ecology do not have a hierarchical relationship. If you work in theoretical ecology you can make analytical modelling or numerical (computer) modelling. If you work in computational biology you could analyze data in genetics, you could model cell processes, you could simulate interacting populations in ecology and many other things.
What should you chose?
What skills do you need?

Do you like data analysis (statistics and R and python coding)? You will have to analyze your data whatever you chose!

Do you like numerical simulations (lots of coding, incl. languages like C++)? If no, then maybe avoid computational ecology!

Do you like analytical modelling (lots of math)? If no, then maybe avoid making analytical models in ecology!

Do you like messy, complicated, tiring field work? if not, then maybe avoid working as a field ecologist.

What would you imagine to work on?

What question would you like an answer to? Think about it and try to understand how you would address the question you are trying to answer.

My advice

Do not be afraid of any field, any technics, any programming language, etc... You are good enough and have enough time to learn what you do not know.

Do whatever you like most!

thank you for the answer. I am surely interested in analytical modelling. But at the moment I can only choose between field ecology and  computational biology (studying metagenomics) and am in a fix as to what will be the most effective option.

Oh ok... that phrasing sounds a little different from the original post. It seems that you know what you want (mathematical modelling in ecology) and are wondering what path will be best to reach this point. I would rather recommend computational biology and genomic data analyses as to stay in a field of theory related work. Note, I am a theoretician (using numerical modelling and not so much analytical modelling) and I would not want my preference to affect my answer. Good luck!

Thanks again:) It's always great to get advice from experts!

Feels like too much of a compliment. I am just a PhD student. I work in population genetics, not in ecology (might have been unclear from above).

I think knowing some statistics and R is good no matter what you're doing, mainly because scrolling past the statistical inferences in a paper (what's a p-value and a confidence interval? How'd they get those?!) feels bad, and the packages you can get add a lot of utility. Edx has am interesting course track on data analysis for life sciences, PH525, that can be taken for free with no obligations if you want to dive into something relevant and get a feel for some methods.

Just a warning on that edX, it's not necessarily beginner/entry so they do assume you know a thing or two about stats, R, molecular biology and related, etc. to begin with!


text:
Male-Male competition limited to breeding season?
I'm currently reading about sexual selection in the context of evolution. Unfortunately, the focus is always on animal behavior during the breeding season. What is 'normal' behavior outside of breeding season?
For instance: Red deer compete with their antlers. Are they doing that throughout the whole year, or just specifically during breeding season?
More general: Does male-male competition exist outside of breeding season?

It's strongest in the breeding season but male-male competition exists outside of the breeding season too, e.g. European Robins only breed in the summer, yet maintain territories year-round. It's pretty circumstantial, however sexual competition will only exist in the breeding season.
To address the Red Deer example, the deer only compete with antlers in the breeding season, but outside of the breeding season they aggregate in same-sex groups too, so most of the competition males will experience is male-male.
Normal behaviour will depend again on the species. Most birds I can think of have discrete breeding seasons and behaviour outside of this is rarely dependent on sex, generally including foraging etc. However I can think of many examples to this, such as Capercaillie, where the hens sometimes forage together. I suppose that 'normal' behaviour could be defined as any behaviour that is not part of the organism's motivation to reproduce.


text:
Are ITS1 and ITS2 good for divergence time estimation?
I had a discussion with a colleague who told me internal transcribed spacers (ITSs) are not good for divergence time estimation:

Because they are non protein coding genes;
Because they belong to a gene family.

However, I was not able to find anything in the literature about that. Can someone please enlighten me?


text:
Estimating population divergence time with a single mitochondrial marker
Is it possible to estimate population divergence time with a single mitochondrial marker?
Here is additional information for my specific case:

Mitochondrial marker: Cytochrome Oxidase Subunit 1 (COI)
Molecular clock rate for COI for my taxon of interest: 1.29-1.96 % per million year
Age of the taxon: ca. 2.69 million years
Number of individuals per population: 10

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


text:
Gene flow analysis with a single mitochondrial marker
I am currently studying a mud snail genus called Ecrobia. Several species of this genus occur in both the Mediterranean and Black seas. Therefore, I would like to investigate whether there is:

Intraspecifc gene flow between the Mediterranean and Black sea populations
Interspecific gene flow between the Ecrobia spp. occurring in the same water body

Therefore, I have a couple of questions:

Is it possible to perform a gene flow analysis with a single mitochondrial marker (COI)? If so, which program could I use to run the analysis?
Ideally, how many individuals per population are required? If I don’t have enough individuals, is there a rigorous way of clustering populations?


text:
Comparing the role of fathers in different species
In species where the male of the species is involved with the life of his offspring in what species is the role he takes is the same as the role of the mother, and in which species is it overlapping or distinct?

Wikipedia estimates there are 2.16 million described animal species and 7.77 million total. So, it seems an answer to your question is going to be quite long. Can you narrow/focus it a bit more?

Maybe take a quick look at wikipedia to start answering your question.

There was a magnificent book that looked at the role of females in several primate species.  it's not new.  the title is "The Woman that never Evolved" The Author, Sarah Hrdy decided to compare the gender roles of various near relatives to imagine how human societies could have been different.  Hrdy also wrote another book on Motherhood.  I'm sure there are many books on fatherhood but I like starting here for a couple of reasons.
By comparing these diverse primate societies she turned on its head previous generations of primatology that had imagined all near relatives live like humans do with a male hierarchy dictating social structure.  not only did she expand our concept of primate social structures, but she also made a statement that human society could be different.  Which, since then it has changed.
There are many diverse studies looking at male roles in primates but this is a good place to start to look at the roles of males.  Its a good comparative structure.  if you are interested in broader sorts of structures, there are so many species and different families you could start... you would have to pick one i'd think.

thanks so much! i'll get those books

This does seem useful to the OP, but I'm failing to see how it answers the actual question asked.


text:
Where are epitopes located on HLA molecules?
Normally HLA molecules present cellular and extra cellular proteins to the immune system; presumably the proteins in this case are where antibody /t-cells etc bind.
But when an organ is transplanted to a HLA incompatible recipient, are they binding to the HLA molecule itself? If antibody response was reliant on the proteome expressed in and around the cell HLA incompatibility wouldn't be such a problem.
What about auto immune diseases?

Your question is both unclear and quite broad. "presumably the proteins in this case are where antibody /t-cells etc bind." Please expand on this, I really don't know what you mean. "But when an organ is transplanted to a HLA incompatible recipient, are they binding to the HLA molecule itself?" What do you mean by they? "If antibody response was reliant on the proteome expressed in and around the cell HLA incompatibility wouldn't be such a problem." Why do you think that? "What about auto immune diseases?" What about them? Please [edit] your question to make it clearer.

@MattDMo the question is pretty clear, he's using correct terminology for the topic

@iayork I'm an immunologist, and I don't really think it's clear at all. In the first sentence, the OP is mixing antibody and HLA/TCR epitopes, and it's not clear which is being discussed where. "are they binding..." is definitely unclear, I don't know what "they" is. I don't understand the reasoning behind the 2nd sentence in the 2nd paragraph. Finally, the last sentence is completely apropos of nothing - what about autoimmunity? The whole thing is unclear and far too broad.

Seems clear to me (also an immunologist).  He's asking how transplant non-self MHC is recognized (peptide dependent or not) and how autoimmune MHC is recognized (peptide dependent or not).  Good questions, if rather basic, and worth addressing.

@mattdmo you rightly picked up on my confusion. I work with hla antibody, but am a mathematician by background. Most of the material I can find doesn't seem to make clear where the epitopes are located. I am not sure if hla antibody bind to the same epitopes as the t cells or to others entirety. So if you want more clarity, I am interested in the locations of the binding sites of either.

@Abijah HLA antibody, meaning antibody that binds HLA? Mostly it binds in regions other than where the peptide epitope is, but there are a handful that bind to the combination of peptide epitope plus HLA, and therefore recognize only the specific combination of HLA plus peptide epitope

Thanks so much- I think that finally makes sense! Thanks for all your help

T cells in a graft see both non-self peptides associated with the non-self HLA molecules, and can also see the non-self HLA molecules regardless of peptide. (MHC is a broader term than HLA, and I will use MHC here.)

Surface expression of CD4 or CD8 is commonly used to identify T-cell subsets that recognize antigen presented by class II MHC or class I MHC, respectively. This holds true for T cells that respond to allogeneic MHC molecules that are directly recognized as foreign, as well as peptides from allogeneic MHC molecules that are indirectly presented by self MHC molecules.

--Contrasting Alloreactive CD4+ and CD8+ T Cells: There's More to It Than MHC Restriction
Recall that as T cells mature in the thymus, they undergo negative selection such that those T cells that spontaneously recognize self MHC molecules are deleted, but there's also positive selection that ensures the T cells can recognize MHC features in general. That leaves many T cells that could spontaneously recognize slightly different MHC molecules (i.e. non-self) that are not deleted. That means that in a transplant, there are a large number of T cells that can recognize the non-self MHC in a non-peptide-dependent manner.  There's also a much smaller number that can interact with the non-self-MHC but only in a peptide-dependent manner; this is just by chance, in that that particular T cell receptor happened to have the shape that sees that non-self-MHC and the peptide.
As for autoimmunity, that's all peptide-dependent, as far as we know, barring some of the really horrendous infant-onset autoimmunities that result from improper T cell maturation in the thymus.


text:
What negative effects does cannabalism have in other species (like prion diseases) and how are they mitigated?
It is well known that human cannibals are likely to suffer from a variety of ailments, particularly prion diseases.
However a great many other species, from insect to ape practice cannibalism at much higher rates.
Do they suffer from similar diseases as a result of their cannibalism? If not why not? and do they have evolved mechanisms for dealing with these negative effects?

First, to be clear, the very act of cannibalism does not cause the development of prions, but the consumption of an animal infected with a compatible form of them, particularly when eating nervous or digestive tissue (i.e. the brain, spine, stomach, or intestines).
To directly answer your question, yes, there are other animals that are susceptible to prions diseases when they consume infected members of their own species, or members of compatible carrier species. In the late 80s and 90s, there was a moderate epidemic of Bovine Spongiform Encephalopathy (Mad Cow Disease) that was concluded to have been caused by including bovine parts in cow feeding stock.
A common defense that I know of against infection from the consumption of infected animals is to simply not consume them at all. I know it's not really the answer you were expecting, but indeed, many animals have an active aversion to corpses, notably perceiving the smell of Cadaverine and Putrescine as repulsive. Evidently, a great defense against disease is to just not eat dead or dying things.
I've never heard of insects or arthropods having neurodegenerative prions, and wasn't able to find anything alluding to them having them, but I wouldn't be too surprised if they had other prion diseases that were infectious between them.
Sources:

Matravers et al. FST (2001);17,1-19

Also available at The National Archives

Cadaverine on Wikipedia
Putrescine on Wikipedia
Sacculina on Wikipedia

My guess is that a large part of why animals don't seem to get prion diseases is age. They take a long time to develop, even after eating a lot of prions. Humans live a long time compared to most animals, so they have more opportunity to develop the disease.

Yeast has prions - I'd actually be moderately surprised if arthropods don't, even though we haven't found any yet.

Some of the processes working against cannibalism:

conspecifics (especially similar-aged conspecifics) are likely to be able to fight back effectively, increasing the risk of injury to the would-be cannibal
for organisms with limited dispersal, nearby conspecifics are likely to be closely related; killing them will decrease inclusive fitness
possible spread of disease

However, a theoretical argument by Rudolf and Antonovics (2007) shows that

... group cannibalism, i.e. shared consumption of victims, is a necessary condition for disease spread by cannibalism in the absence of alternative transmission modes. Thus, endemic diseases transmitted predominantly by cannibalism are likely to be rare, except in social organisms that share conspecific prey. These results are consistent with a review of the literature showing that diseases transmitted by cannibalism are infrequent in animals, even though both cannibalism and trophic transmission are very common.

That is, kuru and bovine spongiform encephalopathy ("mad cow disease") are anomalies; they spread effectively because tissue from diseased individuals was eaten by many other individuals - in contrast to the more common ecological situation where a single cannibal eats a single diseased conspecific.


text:
Does communication with new parts of body requires internal changes in brain?
I am not a biological scientist and have low biology knowledges in general, but I want to know some thing.
Most of us probably can't even imagine what it feels the sixth finger to be touched. Because we do not have one. We can't imagine what should we do to move the sixth finger, although we can imagine same for the finger we have.
I can assume, that people with anomaly additional part of body, like finger or even hand, can fully control and feel it, independently and separately from the "trivial" one.
Analogy
Now, let's consider another world for a while. You probably know about USB - it is a protocol for data communication. There can be USB-device with any type of functionality, and USB-port, situated at some another device (PC, for example), where USB-device could be plugged in.
Number of USB ports of some device, where USB-devices could be plugged in (PC, for example) is finite, so if a user already used them, another device can't be used, without changing some PC internals.
But, USB protocol provides a concept of the USB-hub: this is a device, that concentrates multiple usb-devices, it has several USB-ports in the output, that can be used.
So, with such device, user can use even single built-in USB-port with multiple devices. So, although internally, PC provides only one port, the technology itself can provide many devices, without changing internals of host device (PC).
Back to biology
I was thinking: the person, that is born with additional part of body, that completely functionates, can be felt, can be controlled, and the mainly - separately and independently from others, during ontogenesis obtained some "internal", "core" changes somewhere in the brain, or it is just peripheral stuff, i.e. brain provides some analogy of hub functionality?
If second statement is true, that should mean two interesting things:

Theoretically, even for a person born, with 5 fingers we can emulate feelings of the six's finger.
Again, theoretically there can be infinite, or at least pretty big number of degrees of freedom for such feelings.

This is a site in which we attempt to provide objective answers to biological problems faced by our constituency — students and professionals in biology. Your question fails on all criteria. The 100 reputation granted to members of one SE site when posting to another is based on the assumption they are familiar with conduct on SE sites and will respect sites outside their many area of interest. Please do this.

@David, as You write, that my question fails all criteria, I can argue that: 1) why can't I be considered as biology researcher? 2) Why there could not be given objective answer to the question?

@David, 1. Prove that please. Provide the definition of what researcher means, and prove that I do not satisfy the criteria of definition. 2. Because it is not a question - You are wrong from the start. It is question, and it is a question objectively. What does objectivity means? Objectivity - that, which doesn't depends on opinion, on interaction. So, what I wrote is objectively a question, since it satisfies a definition of what question sentence is, and not satisfies what declarative sentence is. What You wrote next is subjectively, since it depends on Your opinion.

I quote "I am not a biological scientist and have low biology knowledges in general".

@David, Fine, I assume, You mean, that since I wrote, that "I am not a biological scientist and have low biology knowledges in general" I could not be a researcher. This statement is wrong, because researcher, for example, according to Cambridge dictionary is: "someone who studies a subject, especially in order to discover new information or reach a new understanding.". If You visit this site tour page, You'll see, that in the middle of the page it is written: "Biology Stack Exchange is a question and answer site for biology researchers, academics, and students" - they are separated.

@David, so if I am not an academic or a student it does not mean, that I could not be a researcher. As for my arguments for Your second complaint (about objective answer), as I can see You did not mention them, so I assume, that You have nothing to oppose.

What types of questions should I avoid asking?. You can either read this and try to understand the modus operandi and ethos of a site on which you are new user, or continue to play the barrack room lawyer or behave as if you had joined an undergraduate debating society. But do make sure you have the last word, which will be easy enough as I have no more to say on this topic.

@David, okay, so we ended up with Your complaints about objectivity and reasearcher. Now You have next. I have read the link You provided, and some further included links. Please quote exact statement that I violated by adding this post, so I could argue, or agree with that.

I think you'd benefit from reading about the concept of "critical periods" - basically, at different times during development, the brain is learning specific tasks, associating sensory stimuli and motor actions and more complex things, as well (like comprehending and producing language). Some of these things are best studied in model organisms where we can take it apart, but you can also watch a lot of this development in human infants since they are born so early relative to their developmental progress. A newborn really has no voluntary muscle control in their limbs and trunk at all. Arms and legs flail wildly, and only over time do their brains learn and refine how to control those limbs.
I would drop the USB analogy entirely, I don't think it's helping you at all in this case.
Experimentally, it's a bit of a challenge to just "add on" new limbs; it's not like you can tape a new digit on a hand because the developmental processes that connect the nervous system to a digit happen while that digit is growing. The nervous system connections are being made at the same time that the limb or digit is growing. However, there has been study of what happens when you take something away: taping digits together, for example, creates a unified representation in the brain. Occluding one eye causes the brain to use the remaining eye for the entire visual cortex. Some of these experiments are described in this Wikipedia article. These experiments tell us something about the relationship between the brain and the rest of the body: brain regions are dedicated to the parts of the body that sensory stimuli and motor connections are available from. They do not have a pre-ordained accounting of exactly how many or where those sources of information are at, when you take away things that are normally present, brain regions are proportionally dedicated to whatever inputs and outputs are available.
Conceptually, rather than thinking about extra parts, all of your same questions apply just as much to what is "normal". There is no evidence that brain development has any assumption built in that there will be 4 limbs or 5 digits on a hand, rather, connections are made with the nervous system as the limbs and digits develop, and these connections carry information between the CNS and sensory neurons and motor neurons, and the brain develops in response to those connections.

I got the third paragraph of the answer, but in the first one, it seems there is some misunderstanding from You, or from me. It seems to me, like You appeal to concept\part of brain not like some deterministic biological machine, but rather to a "personality", something, that learns after being born (sorry, I probably expressed what I wanted to write badly). I meant, as well as You wrote next, that fingers, skin surface on them, anyway (as I understand) at the time baby is born (comes out from mother normally) already are connected to the brain.

Probably we can consider a spine as USB-hub, but I asked rather about something more internal, i.e. brain: where all of the "connections" from body comes from to the brain - is there are kinda like sockets, and all "connections" from different parts of body have dedicated socket for, so they all connected separately, or there is one interface in the brain, where all connections come to, sending data maybe on a queue, or maybe all it ones generate some superposition data signal and brain decodes and selects from it many different "packets"?

And the third thing - I did not consider any specific part of the living, i.e. when the brain (human) is developing, not being born yet, or already being born, but rather when a baby is already born and grown.

@Stdugnd4ikbd I don't know what you mean by "personality", but the way we use the word "personality" in neuroscience and psychology it does not mean "learned after being born". Lots of things that are not personality, including motor control, are learned after being born, but a lot of learning happens before birth, too. "Learning" in a biological sense is all of the "software" that the CNS operates on; it is all learned.

@Stdugnd4ikbd I think you are taking the computer/brain analogy way too far (this is very common, you're not the only one to do it). You will be much better off starting from scratch, reading about brain development and biology, rather than taking everything you know about how a computer works and trying to find the biological equivalent. There's so much different in the architecture that it just won't help beyond an extremely abstract level.

I absolutely agree, that I need to learn something to understand something, however, I consider it as the case, when a generalized question can be ansked, and generalized answer can be given, the way both understand each other. So, summarise: can feelings of additional parts of body, like sixth finger, or generally, any kind of feelings, experience, can be simulated for a grown person, that already walks, talks, works, etc.? Clarify: I am not interested in will it possibly be difficult to achieve or not. I am interested in is it possible or not

(Additional comment) 1. I've just read critical period Wikipedia article, You provide, it was really interesting, but I rather meant "adding new feeling" not naturally, but artificially, "in vitro". Not as the result of natural development, studying, learning, etc., but forcely

So, if consider critical period conception, it seems like USB-hub analogy is not proper, and the correct is that internal "CPU" changes are needed to interact with new "device". Or maybe not, or true is another variation at all. I will read the article once again tomorrow.

@Stdugnd4ikbd What do you mean "simulated for"? In biology we almost never can speak of what is possible versus impossible; it's definitely possible if it's been done before, but can never be said to be impossible, the best that can be said is "hasn't been done". It's hard enough to regain neural control of a limb which has had neural connections severed yet that the CNS is already familiar with, let alone adding a new part, yet at the same time there are many ways we can learn to interact through existing motor systems to entirely new appendages, like a tool or vehicle.

The former (reconnecting a limb) requires plasticity in the periphery: physical neural connections between the CNS and the peripheral appendage. The latter (driving a car, using a new tool) requires plasticity in the brain.


text:
What is the use of crystallized Photosystems from cyanobacteria?
I read a lot of articles about techniques for the crystallization of Photosystem I and II from cyanobacteria. My question is what is the reason for that and what can you do with Photosystem crystals?

The main purpose of crystallizing a molecule or molecular complex like a  Photosystem is usually to provide a crystal for X-ray crystallography.  A crystal has its molecular components arranged in a structured systematic repeating pattern, and this repeated pattern allows the X-rays to reveal the 3-dimensional shape of one of the components.  Knowing the shape is of biological interest as it suggests how the molecules perform their function.


text:
What is the instructional language of DNA?

DNA carries most of the genetic instructions used in the development, functioning and reproduction of all known living organisms and many viruses (Wikipedia).

Is it already know how ATCG's sequences create theses instructions? Or equivalently, what is the instructional language of DNA? My interest in this question is to know if we already understand how ATCG's sequences can create, for example, human epidermis with an excess of a determined mineral or change cell's shape for more fundamental geometrical ones (triangles, rectangles, diamonds, etc.).
Please, forgive me for this foolish question: I'm not a biologist.

I think the general dogma is that DNA is transcribed to RNA which is translated to Proteins. Proteins have various functions such as the assistance in creating and destroying cells, providing structure, sending signals to the body, and so on. The DNA is the ATCG's.

This is more difficult than it looks. Developmental/Systems/Structural/Etc. Biology are rapidly evolving fields with a lot left unanswered. The answer to that question is probably extremely interdisciplinary and complex.

There are multiple questions stacked on one question. Each one separate look OK.  Consider splitting them up.

This language is called the genetic code. But before talking about this specific code, it is important to talk about how the code is read. Please note that the below answer is a simplification of the reality.
Mechanism by which the code is read
To make things easier (reality is a little more complicated), DNA is "formatted" into RNA which is then "formatted" into proteins. When "formatting" occurs, we do not lose the previous format but we only copied the information into a new format. The formatting from DNA to RNA is called transcription and the formatting from RNA to proteins is called translation.
Proteins are the active units that affect cell activities. The activity of the proteins is a function of their sequence. As a consequence the language/code we must understand is the relationship between DNA and proteins.
Numeral systems of DNA
DNA, as you said, is written in quaternary (=numeric system at base 4). The four letters are called A, T, C and G which stands for Adenine, Thymine, Cytosine and Guanine (4 nucleotides).
Numeral systems of proteins
Proteins, on the other hand, are coded in a system at base 21 (21 amino acids).
Redundancy
Because $4^2=16<21$, we need to use (at least) 3 letters in DNA to code for 1 amino acid. Because $4^3=64>21$, we necessarily have several codes of 3 nucleotides that match to the same amino acid. We talk about redundancy. In computer science, a byte is a series of 8 bits. In biology, a codon is a series of 3 nucleotides.
Code
Below is the code:

, where Phe, Leu, Ser, etc... are an abbreviation for specific amino acids. Phe for example is the phenylallanine.
As you can see in the above table, most of the redundancy is caused by changes in the third letter of the codon. More information on why it is the case on this post.
There are 4 special codons.

AUG: Is the start codon. It is an indication of where translation should start.
UAG, UAA and UGA are stop codons. They are an indication of where translation should stop.

Possible confusions
Central Dogma of Molecular Biology
The unidirectional relationship between DNA, RNA and proteins has been called Central Dogma of Molecular Biology. Of course, there is no place for dogma in science and the term is very improperly used. Interestingly enough, the Central Dogma of Molecular Biology is partially wrong because this relationship between DNA, RNA and proteins is not necessarily unidirectional. The reverse transcriptase is an enzyme that reformats DNA from RNA.
Genetic code
If you google "genetic code", most hits will display the letter U instead of the letter T. The reason is that the code is often presented for the relationship between RNA and DNA and the only difference in the code between RNA and DNA is that T (Thymine) is replaced by U (Uracile).
mRNA vs RNA
Not all RNA are meant to be translated into proteins. Only mRNA (m stands for "messenger") are. For example, the process of translation is itself catalyzed by RNA (called rRNA, where "r" stands for "ribosomial")
Note also that DNA is first transcribed into pre-mRNA which is then modified into mRNA before being translated.
Is all of DNA transcribed?
No. In eukaryotes (which include pretty much all the living things you may think of to the exception of bacteria and viruses), most of the DNA is not transcribed. The rest is used for regulatory purposes or might not be used at all. The regions (called locus/loci) of the DNA that is being transcribed are called genes

Nice answer! +1. You might want to add little bit about developmental biology, French flag model etc to touch OP's question about cell shape and geometry.

Not to mention epigenetics

The genetic code is a hash table, not a language.

@David Sure.... A dictionary is a hash table too. Note that I used the term language in the informal sense and mainly because OP used this same term.

Too many poor questions receive poor answers imho because the respondents do not challenge the false assumptions in the questions. A dictionary is not enough to define a language; it needs a grammar too.

The functions of DNA and proteins are determined by their shape, and while their shape is mostly determined by their sequence, there is no computational way to design proteins from scratch to do whatever we want.  The modeling is just too complex.


text:
How the genome assembly be done after k-mer counting?
As far I know, before assembly of a genome, all k-mers from read should be counted.

But after that, how the genome assembly be done?
Is there any other thing needed along with k-mer counts?
How the standard value of k is determined for a particular genome assembly? or is it fixed for all kind of assembly?

I just want to know the basic concept that how this actually been done. Explanation with flow char or algorithm is much more appreciated.
I went through some similar question, but those did not help me too much.

There are multiple ways of doing genome assembly.
The term you are probably looking for is "De Bruijn-Graph based assembly". Using this you can find a lot more different explanations of how it is done.
Another frequently used method is "Overlap Layout Consensus assembly", which in fact is not based on k-mer counting.


text:
Is studying complete mitochondrial genome need biological lab work?
The research complete mitochondrial genome study done on species:

Juema pig Sus scrofa (Suina: Suidae) from southern Gansu
red rainbowfish
speckled dace, Rhinichthys osculus
white char Salvelinus albus (Salmoniformes, Salmonidae)
Himalayan honey bee, Apis laboriosa

Did they need to do any work in biological laboratory?
More specifically, Are they related to bioinformatics completely?
Most of them just wrote length in bp (base pair), percentage of ATGC and several combinations of them and some special behavior. These seemed to me as expressing some statistics.
So, how could it be a research work?

All papers you mentioned have involved biological lab work. They all have sequences specific mitochondrial genome and then have analyzed it with the help of bioinformatics. Sequencing genome requires lot of bench work (wet work or "biological lab work"). Even one of them have mentioned it in abstract itself.

The complete mitochondrial genome of Himalayan bee Apis laboriosa, from Mizoram, India, has been sequenced using Illumina NextSeq500 platform and analysed.

Yes, obviously there should some biological lab work. but is it possible to do this types of thesis without doing the biological lab work practically? say collecting the lab work data from any open source gene bank or something. You know, a lot of bioinformatics thesis could be done without doing any biological lab work. can it be done that way? (Sorry for my bad English. I asked one question here, but several questions appearing to make you understand the question)

@manetsus Someone needs to do the lab work to generate the data for analysis by bioinformatics. That's not always the person doing the analysis, but even then they must have a very strong understanding of biology in order to create relevant conclusions. The best way to learn biology is by doing.

@MattDMo I fully agree with you. but my question is the one who just doing analysis on the basis of lab work available on the internet is producing knowledge or not?

@manetsus if you are making novel insights into biological phenomena, then of course you are producing knowledge, regardless of whether you have a pipettor or a computer mouse in your hand. Just look at the fields of mathematics and theoretical physics - a lot of work is done without ever being able to do experiments at all.

@manetsus, Yes that is possible. You can join any theory, bioinformatics, systems biology or computational biology lab. These don't required wet work. These fields are also in demand now a days.


text:
Apical meristem regrowth?
When the shoot apical meristem is cut out/removed, it induces lateral growth. I'm wondering if this means that that stem will never grow vertically again. Is there a way to stop lateral growth after the apical meristem is removed? Is there a way to grow that meristem back again?
Thank you

what plant? Different plants will give you very different answers here


text:
Can organisms like Noctiluca be commercially exploited?
Scientists think that Noctiluca flashes to startle or scare away its predators. The bioluminescence might also attract bigger predators to eat Noctiluca’s predators, just like a burglar alarm that alerts the police to come to someone’s house to catch a robber.
 It takes energy to make the chemicals that allow them to glow. It would be a waste of that energy to glow during the daytime
But the question is whether we can commercially exploit this for human welfare??

Well, scientists have been developing Bioluminescent Plants to use as a future road light source. Also, there is a way that Bioluminecent algae can be used as medicine.


text:
Do Type 1 (Slow Oxidative) muscle fibers also make use of glycolysis?
I'm aware that slow-twitch fibers make use of oxidative phosphorylation; however, I am unsure if this is done in conjunction with glycolysis and the krebs cycle? Do these muscle fibers go through all three stages of aerobic respiration, or just the final step? If not, where are they getting the precursors for oxidative phosphorylation (NADH, FADH2)? Would they use fatty acids and proteins as precursors in the krebs cycle (if applicable)?
Slow-twitch (Type IIB) seem to use glycolysis and then anaerobic respiration (forming lactate), right?
Any input is greatly appreciated!


text:
Is Hemoglobin binding to oxygen the same as Adsorption
I have recently been reading about Hemoglobin and came across how it binds to oxygen. This seems very similar to Adsorption. Is the process of Hemoglobin binding to oxygen through Adsorption ?

I’m not about expert on this topic but from what I know the binding of oxygen to heme groups is a phenomenon of complexation, not adsorption.

From the Wikipedia article you cite the answer to your question is clearly NO. They seem very different: absorption is described as a surface phenomenon, whereas oxygen binding occurs in a single internal pocket in each globin subunit and forms a specific bond to an Fe(II) atom. The chemical nature of this pocket is quite different from that of the surface of the protein.
The Wikipedia article states:

Adsorption is the adhesion of atoms, ions, or molecules from a gas, liquid, or dissolved solid to a surface.[1] This process creates a film of the adsorbate on the surface of the adsorbent.

and

Similar to surface tension, adsorption is a consequence of surface energy. In a bulk material, all the bonding requirements (be they ionic, covalent, or metallic) of the constituent atoms of the material are filled by other atoms in the material. However, atoms on the surface of the adsorbent are not wholly surrounded by other adsorbent atoms and therefore can attract adsorbates.

However if you consult a text-book which describes the biochemistry of haemoglobin, such as Berg et al. you will find the specific chemical nature of the binding clearly described, as indicated by this extract:

The iron atom lies in the center of the protoporphyrin, bonded to the four pyrrole nitrogen atoms. Under normal conditions, the iron is in the ferrous (Fe2+) oxidation state. The iron ion can form two additional bonds, one on each side of the heme plane. These binding sites are called the fifth and sixth coordination sites. In hemoglobin, the fifth coordination site is occupied by the imidazole ring of a histidine residue from the protein. In deoxyhemoglobin, the sixth coordination site remains unoccupied...The binding of the oxygen molecule at the sixth coordination site of the iron ion substantially rearranges the electrons within the iron so that the ion becomes effectively smaller, allowing it to move into the plane of the porphyrin (Figure 10.19).

The only similarity I can see is that in both processes the interaction of the gas with the material to which it binds is controlled by the pressure of the gas. However in the case of haemoglobin there is a distinct difference from absorption in that the dependency on pressure exhibits a sigmoidal curve, specifically suiting it for the role of quantitative delivery of oxygen to the tissues at a particular small reduced pressure range.
You sound as if you come from the physical sciences. If so, prepare to be surprised at how smart a chemist Mother Nature is.


text:
How does dsDNA become ssDNA when binding to a nitrocellulose membrane?
I would like to know how double stranded DNA becomes single stranded when binding to nitrocellulose membrane in southern blots. Does it require a special reagent? Is denaturing a special property of the membrane itself?

The DNA is denatured in-gel prior to transfer using alkali conditions, most commonly a solution containing 0.5 M NaOH (buffered with 1.5 M NaCl). Following that the pH of the gel is neutralised in 0.5 M Tris-HCl, pH 7.5; 1.5 M NaCl.
I have found the Roche DIG application manual to be a well-written and reliable resource for performing Southern and Northern blots. The section on Southern blots starts at page 94 and you can modify the protocol to suit other detection systems.

No, there is no such property present in membrane. After transferring to membrane they treat with alkaline solution to denture dsDNA to ssDNA for binding of probe.

Don't most transfer methods only allow ssDNA to transfer from the gel to the membrane?


text:
How do nasal and aural passages connect?
I have had a bad flu with a lot of congestion.  My husband suggests a way to clear my stuffed ears is to pinch my nose shut then blow air through.  Sometimes that helps, sometimes there's just too much congestion.
What is happening exactly when I do that?  I've looked at diagrams of nasal and aural passages, but it's not clear to me what's happening when you block the nasal passage and then blow air through.  I would like to know exactly what the passage of air/fluid is.
Also, is it a bad idea to do it?
Thank you.

The eustachian tube connects the nasopharynx to the middle ear, on each side. The (naso)pharynx is basically the back of the mouth, and the middle ear is a cavity behing the eardum.
https://en.wikipedia.org/wiki/Eustachian_tube
It is normally closed when there is no pressure difference between the middle ear and the nasopharynx, by extension between the middle ear and the air around one. Its function is to avoid a ruptured eardrum that could be caused by such difference in pressure. (This could be the case when ascending a mountain, or diving underwater, where the ambient pressure drops or increase, but not the pressure inside the middle ear)
What you are doing is closing all passages for the air to flow out (mouth and nose closed), yet trying to blow it out : this artificially increase the pressure and opens the tubes. While it is usually a passage for air, if there is a fluid buildup it could flow through it too.
Whether it is safe is a more of a medical question, which would be better suited for your physician.

Good answer, but please do not provide any sort of medical advice on this site. Instead, encourage them to ask their physician.

Thank you very much for your very helpful answer, much appreciated.

The Eustachian tube, also called the auditory tube (or canal) connects the middle ear to the nasopharynx (the back of the nasal cavity):

From Brigham and Women's Faulkner Hospital
Here is where it connects:

From Wikimedia

@AlwaysConfused that is correct. The nasopharynx is in the back of the nasal cavity, and the opening of the auditory tube is some distance above the soft palate, so there is no way of seeing it through the mouth. The back of the mouth is called the oropharynx (oro- being derived from oral). Pharynx is a general term for the tissue at the back of the throat, stretching from the nasal cavity (nasopharynx) to the mouth to the larynx (laryngopharynx) just above the split between the esophagus to the stomach and the trachea to the lungs (which actually contains the larynx).

Thank you very much for these wonderful diagrams, very helpful in allowing me to visualize it.  Thank you.


text:
Can I force evolution in a group of cells by removing all the smaller cells?
I actually have algae growing in water in a container. I was thinking if it was possible to filter the water so that all the small cells will be filtered out and only the bigger ones will remain to reproduce cells that tend to be bigger.
Is that possible?
What type of filter should I use?

A formal showing of your 'selection pressure' might also require proof that your initial algae population consists of only 1 type of algae.

Wouldn't this actually be artificial selection?

@evamvid which is a form of evolution.

Short answer
Yes that would work in the condition that the trait you select for (size) is heritable.
Long answer
The kind of selection you would apply is called truncated selection because you fix a limit in size (depends on your filter) under which individuals do not survive and above which individuals survive and reproduce equally.
The response to selection ($R$) is given by the breeder's equation:
$R = h_N S$
, where $S$ is the selection you apply. In your case, $S$ is the difference between the mean size of the parent generations and the mean size of those you allow to reproduce in the parent generations. $h_N$ is the heritability (more info in additional info).
So, if you measure the mean size of your cells, filter them, measure their size again (or infer their size based on previous measurement and the size of you filter) and calculate the difference between the two measurements you get $S$. Then you let your filtered individuals to reproduce and you measure the size of their offspring which is $R$. By dividing $R$ by $S$ you get the heritability $h_N$. If you do not observe any difference in size between your two generations it means that the heritability is 0 ($\space h_N = 0\space$). Of course, you'll need a population that is composed of enough cells in order to have a good estimate.
Additional info
To be a bit more accurate $h_N$ is the heritability in the narrow sense. It represents the part of variance in the population that has to be accounted to additive genetic variance. The word additive genetic variance might seem obscure. In other words
$$h_N = \frac{V_{Ga}}{V_{P}} = \frac{V_{Ga}}{V_{G}+V_{E}} =  \frac{V_{Ga}}{V_{Ga} + V_{Gd}+V_{E}}$$
, where $V_{GA}$ is the additive genetic variance, $V_{GD}$ is the dominance genetic variance, $V_E$ is the variance due to environmental variance and $V_P$ is the total variance (phenotypic variance)
Hope that helps. Do not hesitate to ask further question if something is unclear or if I missed one of your point.
Edit
Filter
The filter you need should allow you to discriminate the cells based on their size. Therefore, it should be relatively accurate. It is common to classify the phytoplankton based on their size, see this. You should try different filters and see what filter allows a good discrimination.
EDIT
I assumed your cells were all of the same species. Is it the case? If you just sampled them from a lake and let them grow in a container then you very probably have various species. Therefore, you would select (based on their size) for species with your filter rather than selecting individuals within a species (based on their size again). It is kind of the same process anyway and the breeder's equation still holds.

thanks for the very helpful answer. can you tell me what filter i can use?

@SumitSingh See my updated answer.

I just saw your edit re single species after I had commented the question.  OP sounds like a fun science project, if it can be performed accurately!

I think one would not have a lot of success using a filter to do this, rather using a centrifugal gradient and comparing the fractions to a standard I think would be preferable. Nitrocellulose filters are made with precision but not very astounding accuracy which is the main reason they are commonly used at set sizes (like 0.2 and 0.4 microns) and not often in between. Good question though


text:
Percentage of understood human DNA
I want to know what's the approximate percentage of understood human DNA, as in, which part does what. I'm not asking for details, just the amount.
Thank you.

I am not sure if this can be said. Understanding the human genome is a process still going on today. Additionally this field is moving rather fast.

You would need to define "understanding". This is not a book where we simply have to read the words. Each "word" can have multiple different functions and we can't say with complete certainty that we understand any of them 100%. We have a pretty good idea about a relatively large part of it but understand is a loaded word.

Thank you. So if I understand this, DNA is being deciphered. But, we still can't say for certain that we know what each part exactly mean. Is that correct?

The devil is in the details, and therefore we cannot just state that we have understood X% of the DNA. We know e.g. that 2% of the human DNA encode proteins. And for a good number of proteins we know what they do. So you might know that a particular codon AGT encodes a serine residue in a protein, which could have a catalytic activity. Or it has a structural activity. Or we are not sure what it does. Sometimes protein-coding and regulatory sequences overlap. So even if we first understood the protein-coding function, there was still the regulatory function to be discovered.
The upshot is that there are multiple levels of understanding, and big controversies of what they actually imply (see e.g. the ENCODE saga).

Okay, I didn't understand your example but I got what you meant by it. Your answer was satisfactory. Thank you. You also gave me something interesting to read about.


text:
When does exposure to an allergen increase / decrease allergy?
In immunotherapy a person is regularly exposed to an allergen to decrease the allergy. Yet apparently "repeated intranasal challenges ... induces robust allergic airway inflammation, " [0]
So when does exposure to an allergen cause allergy induction vs hyposensitization?
[0] http://www.researchgate.net/post/Which_is_the_best_way_to_sensitize_mice_to_house_dust_mites

Small or relatively small amounts of the antigen can cause an allergy, when you have IgE antibodies which fit to this antigen. They will then cause a local immune reaction and cause the secretion of histamine.
For the desensitation therapy large amounts of antigen are given (which is not without risk). The mechanism behind this therapy is not completely understood, but there are some good points.
The immunetherapy seems to induce class switching from the IgE antibodies which can trigger allergic reaction to IgG who can not do this. Furthermore the IgG will mark the antigen for uptake and degradation by the mast cells.
This seems to be induced by a shift from a Th2 immune response over to a Th1 response. This also leads to the production of a different set of cytokines which are anti-inflammatory (IL-10 for example) and the already mentioned different secondary immune response. The immunetherapy reduces the amount of mast cells, basophils and eosinophils which are recruited into skin, nose, eye and the bronchial mucosa. These cell usually support the reaction to allergens in this tissues after the exposure.
See these papers for more information:

Allergen immunotherapy.
Allergen-specific immunotherapy


text:
In the endomembrane system, after a protein leaves the rough ER, where does it go?
It can either go to the smooth ER then to the Golgi or it can go directly to the Golgi, right? Also, the smooth ER gets all of its material to synthesize things from the rough ER, right? Sorry, I looked around but couldn't really find a direct answer to my question. Thanks!

I'm no expert at this but will do my best to answer your question based on the title. It depends on the protein! proteins can either be cytoplasmic, nuclear, transmembrane or secretory. Cytoplasmic proteins (as far as I know) get released to the cytoplasm after they have been folded correctly (through chaperones) and gone through the quality control mechanism. Nuclear proteins get transported through the nuclear pores, across the nuclear envelope through chaperones. Now for the transmembrane or secretory proteins, the fate of these proteins and where they go is decided by the ER (but obviously the information is there in the protein sequence). Transmembrane proteins have a signalling peptide and a transmembrane domain signal anchor sequence which ER recognises and through fancy looping and elongation across the ER membrane, the proteins is further translated by the ribosomes and eventually gets translocated to the cell membrane. There is very very nice nature review paper (Rapoport, 2007) about this and if you look at Figure 5, you will get a good ideas as to what goes on. For the secretory protein again its the interaction of the protein sequence with the ER membrane, helped with the ribosomes (in fact the groves in the ribosomes are key for making these fancy looping happen as the protein residues in ribosomes interact with peptide residues (amino acids) that are being produced on the fly), that processes it and sends it for secretion (Rapoport, 2007) and trans-golgi network is also important in the secretion process (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1424219/).
Hopefully these information would provide you with some hints.

there are also scads of poorly or uncharacterized lipid compartments within the cell.  I'm not sure we can even name them all, but the proteosome is an example, as are the vescicles that recycle receptors like insulin receptor within the cell.


text:
Do miRNA and antisense RNA do essentially the same thing?
Don't they both just disrupt RNA so it can't make a protein? If so, then what is the difference between the 2?

Antisense simply means that a sequence is the complement of another. miRNAs are naturally occurring antisense RNAs yes. The "difference" is that antisense RNA is often used for sequences developed in the lab and used for processes such as RNAi.
miRNAs, on the other hand, are encoded by the genome and are used by the cell for regulating gene expression. They do this through the RISC complex, just like artificial antisense RNAs such as siRNAs.
Basically, antisense is the general term, and can be applied to any sequence whose complement exists in the genome. miRNAs are a particular class of antisense RNAs.

@guest you're very welcome. If this answer solves your issue please take a minute and check the check mark under the vote count to the left, this will signify to everyone that your issue's been resolved.

Antisense RNA is any RNA that is complementary to another RNA. Therefore, miRNA is a type of antisense RNA. Antisense RNA can inhibit translation of mRNA by hybridizing and preventing ribosomal binding/translocation. Antisense RNA in this context could be any length and bind anywhere between the RBS and end of the CDS. miRNA also prevents translation but it does so through the RNAi pathway by facilitating binding of the RISC complex to mRNA (often in the 3'-UTR, which is after the CDS). miRNA are around 22 nts long (but it is species dependent).

Strictly speaking, it does not need to be complementary to mRNA. It can be complementary to any RNA moiety.

Thanks! I've updated it. If I had seen your answer I wouldn't have posted but I got sidetracked in the middle of typing mine and it got delayed.

No reason not to post! The more the merrier :)