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Could a person become physically transgender through artificial means?
Let's say there's a girl who carries a few masculine traits not normal in most girls, such as a high level of testosterone; we know there are countless reasons why something like this could happen, but could that girl have actually been concieved as a boy but modified before birth to become almost fully female, with only slight traces of male traits left? Is that possible through any sort of technology, or does biology even work that way?
For instance, if a male baby was injected with high amounts of female hormones before his birth, or really, anything else that could alter his gender, in any case could he start morphing into a girl, even if not fully? (Say, to the extent where he became more of a girl but still possesed a few common but not very specific/clear/exclusively male traits such as excessive body hair, etc.?)

A "high level of testosterone" must be made within the context of a particular sex. Men tend to have much higher levels of testosterone than women, but the testosterone production and levels within women vary widely - just as many hormones. Genetics, environment, diet, drugs, and workout regimes can all affect testosterone levels. A qualified physician will be able to tell where a person is after a test.
As for the rest... Every case of gender reassignment I've heard of and read about has occurred after birth. Read through this Johns Hopkins Magazine article from Sept. 2000 to get a fairly good understanding of when gender reassignment occurs and how it's handled. Here's a quick rundown (summaries, NOT quotes from the article):

Inadequate exposure to Testosterone in utero can result in ambiguous genitalia or other conditions such as 'micropenis' for an XY fetus. Up until the 1990's, regardless of chromosomal gender, children with the conditions would be reassigned as 'female' and had reconstructive surgery very early on.
Androgen Insensitivity is when an XY fetus is genetically incapable of utilizing male hormones and can involve several levels of insensitivity from "Complete" to "Partial". Complete insensitivity usually leads to fully feminine genitalia, while "Mild" or "Partial" can lead to partially or fully masculinized genitalia. Genitoplasty is an option for the latter cases.
CAH - congenital adrenal hyperplasia. This genetic disease causes the adrenal glands to produce excess androgens--the steroids that cause masculinization--a process that begins in the womb and can result in ambiguous genitals. However, CAH girls are generally more aggressive and display behavioral tendencies that more closely coincide with boys of the same age. Important to note: CAH children are genetically female (XX) and identify as female.

An extensive review of gender reassignments in 1997 had this to say about the consequences of surgically altering an infant's sex:

Considering this case follow-up, and as far as an extensive literature review can attest, there is no known case where a 46 chromosome, XY male, unequivocally so at birth, has ever easily and fully accepted an imposed life as an androphilic female regardless of the physical and medical intervention.

HOWEVER - as with all things scientific - there is dissent from the Johns Hopkins article above:

Preliminary analysis of the data, says Migeon, indicates that almost all of the patients are content with the gender in which they were raised. All but two showed a gender identity and gender role in accordance with their gender of rearing.

There is significant divergence that has not been reconciled in any trustworthy article I could find. The modern practice is to raise the child as their genetic sex unless significantly afflicted.
In adult transgender individuals, things like Hormone Replacement Therapy are part of a regime - along with surgery, acclimatization courses, and psychological evaluations - that can successfully result in a person presenting themselves and physically resembling another sex.
With adequate surgery, hormone therapy, and proper treatment all-around, it is practically impossible to tell whether a person is transgender without getting invasive or performing genetic tests.
As with all things that veer into a hazy area between medical knowledge (medical advice is not allowed on this website) and human biology: DO NOT use the above information to diagnose yourself or anybody you know. ONLY a qualified medical professional can perform the necessary tests required and give a qualified interpretation of the results.


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What is the life cycle of a wart?
There doesn't seem to be a lot of information available on research done on warts.  What is the life cycle of a wart?  How does it spread? -- specifically how does it recruit cells to spread it?  What is the life cycle of a PV-infected dermal cell?

This article has some good information. It's certainly more than I want to know about warts.

Isolated warts may remain unaltered for
  months or years, or a large number of new lesions
  may develop rapidly in a short period of time. The
  development of warts is not predictable.
  Approximately 65% of warts disappear spontaneously
  within two years. The patient’s age and number of
  lesions do not seem to affect the prognosis.

There are many different types of warts and of HPV. Since warts cause a type of dysplasia their life cycle can be very variable and unpredictable.

Do you mind summarize some of the key points in the article. The link might die someday, and it'd just make a much more complete answer :).

Sure. I'm new to Biology beta. It seems to me that the nature of the site necessitates a lot of linking and referencing since there's no way to confirm someone's credentials. And even those with credentials need to cite their sources.

Welcome :). Generally, when making a claim, a reference is just customary. The edited answer is great though, +1.

Conner's response contained just the type of source material I was looking for.  Thanks Conner -- let us all +1 him.  Allow me to summarize the specifics of the article in relation to my question:
Transmission

PVs are transmitted through direct or indirect contact with an
  individual who has the lesion. Dysfunctions in the epithelial barrier
  by trauma, minor injuries or maceration cause loss of solution of
  continuity in the skin, thus allowing viral infection. After
  inoculation, the incubation period varies from 3 weeks to 8 months.
  Spontaneous regression is observed in most cases.

Infection

Infection begins when the PV reaches the cells of the basal layer;
  there is no viral replication at this location and the virus just
  keeps its genome by amplification of a low number of copies.

Replication

The replicative phase and protein synthesis occur in the suprabasal
  differentiated keratinocytes. Progression time and type of lesion
  correlates with the quantity of viral particles detected. Younger
  warts present a higher viral amount when compared to old warts.
  Plantar warts have a higher viral load than common warts. The center
  of the lesion appears to be the main site of viral concentration.

Latency

PVs appear to remain in their host for long periods of life. A variety
  of different types of PVs can be detected in random sites of normal
  skin in humans and animals. This reinforces that a latent life cycle
  is often a characteristic of these viruses.

Interesting Notes

There are no known PVs that infect more than one species.
To date, about 100 different types of HPVs have been fully characterized.
Human PVs does not grow on conventional culture media. The diagnosis of HPV infection is made by histopathology of lesions

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What is the molecular basis of hangovers?
Well, most of us have experienced the wonderful feeling of the dreaded hangover. How does it work exactly? I imagine it has something to do with dehydration but what are the underlying mechanisms?
Extra points for explaining why mixing drinks makes it worse and why (or if) a hair of the dog (another drink) the next day can help. Someone once told me that hangovers are the first symptoms of withdrawal and if you drink (anecdotal evidence suggests that it should be the same drink as the night before, but I doubt this is true) a small amount of alcohol, the symptoms are alleviated. I don't really see how that can be true.

First, the hormonal and hemodynamic changes seen in hangover are distinct from those seen in alcohol withdrawal, so the advice to drink more is not good, even if some symptoms are in fact improved. See tables 2/3 in the cited review.
It appears the molecular mechanism of veisalgia (HA, a new word) is not well known.
1. acetaldehyde Part of it may be attributed to acetaldehyde but there is clearly more to it. The liver enzyme alcohol dehydrogenase 1 (ADH1) produces acetaldehyde from ethanol, and aldehyde dehydrogenase 2 (ALDH2) makes acetate from that, so the aldehyde does not exist for a long time, and is rather responsible for short-term illnesses.
2. ADH and diuresis

Hangover severity is proportional to antidiuretic hormone
  concentration (46). Alcohol inhibits the effect of antidiuretic
  hormone on the kidneys, thereby inducing  diuresis that is out of
  proportion to the volume of fluid ingested. As blood alcohol
  concentration decreases and dehydration persists, the serum level of
  antidiuretic hormone increases, maintaining water retention in
  dehydrated patients with hangover. In our clinical experience,
  hydration attenuates but does not completely relieve hangover
  symptoms.

3. cytokines

The constellation of hangover symptoms (nausea, headache, diarrhea)
  resembles that seen in conditions related to dysregulated cytokine
  pathways (for example, in viral infections and after administration of
  interferon-alpha). Alcohol alters cytokine production through a
  thromboxane pathway. Levels of thromboxane B2 are elevated during
  experimentally induced alcohol hangover (42), and the administration
  of tolfenamic acid, a prostaglandin inhibitor, at the time of alcohol
  consumption has a small prophylactic effect in reducing hangover
  severity (9).

4. further substances

Congeners, the byproducts of individual alcohol preparations (which
  are found primarily in brandy, wine, tequila, whiskey, and other dark
  liquors), increase the frequency and severity of hangover (24, 39,
  40). Clear liquors, such as rum, vodka, and gin, tend to cause
  hangover less frequently.

So there are factors that aren't even identified exactly, and these could fit the mixing of drinks observation.
There are several reviews out there, just search for hangover at Google Scholar.
Wiese, Jeffrey G., Michael G. Shlipak, and Warren S. Browner. "The alcohol hangover." Ann Intern Med 132.11 (2000): 897-902. Online at http://dionysus.psych.wisc.edu/lit/topics/Hangover/WieseJ2000a.pdf

Thanks for the comprehensive answer, I would have accepted it earlier but I was holding out in case anyone could explain the mixing drinks thang.

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What did Richard Feynman contribute to molecular biology?
Some time ago, I read James Gleick's "Genius: The Life and Science of Richard Feynman", a wonderful biography of Feynman and, by extension, most of modern physics.
In this book, the author mentions that Feynman spent a year working in a biology lab and that during that year he made an important discovery.
I remember that when reading the book as an undergraduate biology student, I knew the discovery in question well enough to be immensely impressed that it had been discovered by someone foreign to the field.
Unfortunately, I no longer have the book and cannot remember what that discovery was. Does anyone know?

Don't know the answer, but this has always made me lough a lot (and I deeply agree with Mr. Feynman)

@nico Tell me about it, the time I spent memorizing the names of all the myosins... I actually had an exam question once, asking what year the Origin of Species was published in. Not what the book said mind you, they were asking for information you can get by looking at the inside cover. This in what, at the time, was the best rated University for Biology in the UK.

According to Gleick, Feynman spent the summer of 1960 in Delbrück's lab at Caltech and discovered intragenic supression.
This is where the expression of a gene which has been knocked out by a mutation may be restored by a second mutation within the same gene.
Fenynman worked with the rII mutant of phage T4 and was looking for back mutations in E.coli strain K.
He noted some unusual plaques which he labelled idiot r's.
Feynman correctly deduced that these revertants were due to a second mutation which cancelled the effect of the first, but he did not publish the result, possibly because he had no molecular explanation for what was going on.
The Delbrück lab referred to these revertants as Feyntrons.
Cricks and co-workers in Cambridge, UK, correctly explained the phenomenon.  If, for example, a mutation caused a gene to be read out of sequence (a frameshift mutation) then a second mutation within the same gene could put the message back 'in phase', thus cancelling out the effect of the first mutation.
All the above is taken from James Gleick (1992) Genius.  Richard Feynman and modern physics, a great book.

That's wonderful, thank you. I have been trying to remember this for years. Are you sure about the book's title though? I can find no reference to it. See my answer for the one I remember and can find.


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Copper for cell incubator to prevent contamination
For some reason the lab seems to have a problem with contamination every so often.  It's virtually impossible to prevent bacteria, viruses, fungi, etc. from getting into the incubator every time you open the door.  Our incubator is pretty old, we don't have one of the new fancier versions that's made with pure copper inside, which effectively kills microorganisms.
Would it be a good idea to buy a copper plate and place it on the shelf, on which we could put our culture flasks?  Or would it disrupt the flow of heat/CO2 too much?  Would it be better to buy copper foil and wrap the shelves in it, then poke holes into it where all the holes are in the shelf?
We use good cell culturing practices; I don't contamination is happening because people don't know what they're doing.  It just happens over time with enough people working in a cell culture room.  Could copper in the incubator help?  We probably don't have the money to buy a brand new incubator that's made out of copper, so would this be a viable, economic alternative?

First thing I'd do is replace the HEPA filter. A copper plate/foil may help, and it certainly won't disrupt the flow of heat, as copper is incredibly conductive (that's why they make electrical wires out of it), and poking holes would help with the airflow, but a new filter will probably make the most difference. I've never used a full-copper incubator, and the few serious contaminations I've had to deal with were related to the HEPA filter and poor TC practices.
If you haven't already, I'd institute a good routine cleaning program as well. Change the water bath each week (make sure you're adding fungicide to the water), and wipe down the whole incubator with bleach followed by an alcohol rinse each month. Make sure you clean all the bleach off, as it corrodes metal if left on very long. At the same time, clean and autoclave all of the removable components like shelves, rails, and water pans.
Good luck!


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PTMs of proteins via mass spec?
I understand that mass spec is widely used to study PTMs like glycosylation of proteins, but how can mass spec determine correct PTM structure of say glycosylation if two glycan structures have the same mass but different arrangement (i.e. isobaric)? Also, how can mass spec determine the difference between structural isomers?

Based on fragmentation patterns.

@WYSIWYG: could you elaborate (in an answer)?

I am not a MassSpec expert but this is what I understand from my spectroscopy basics:
In tandem MS (MS-MS), the ionized analyte generally undergoes or made to undergo fragmentation (breaking up into smaller ions). Fragmentation allows you to study finer details. It is also essential for de-novo peptide sequencing. Different fragmentation techniques, such as Collision Induced Dissociation (CID) or Photofragmentation, yield different kinds of secondary ions.
You can intuitively understand that Fragmentation of structural isomers will yield different kinds of secondary ions (using the same fragmentation technique). The choice of fragmentation technique depends on the molecular nature of the analyte. In the article that I mentioned previously, they use laser induced photofragmentation to dissociate glycan-ions.
Even small molecules, which had been classically studied by MassSpec, undergo isomerization after ionization in order to stabilize the ion. Reactions such as reverse-Diels-Adler can also happen. The pattern of reactions would differ between structural isomers. For basics you can refer to a book on Spectroscopic techniques by Silverstein


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Does anyone know what marsupial this is?

I know what this is a marsupial, but i'm not quite sure which one. Any thoughts?

Why was this closed? Species identification questions seem to be on topic and this is no more localized than any other such question. @mad-scientist?

I think the OP could have included information like where the photo was taken? But still I am inclined to agree - I have seen many similar questions on here that were not closed.

@terdon I closed it mainly because it was self-answered in a very short time and because the question and the answer don't contain much detail

I had not taken the photo myself; I had received it from lecture notes that did not give any information about the photo. The reason I answered in such a short time after posting it was because I had asked an Australian friend of mine, and he got back to me not long after I had asked the question. So I thought it was best I answer it. As for the detail in the answer, the question was just relating the species, nothing else.

I can see how it looks suspicious though! Sorry!

I've been told it is the marsupial 'Myrmecobius fasciatus' commonly known as the numbat.
http://en.wikipedia.org/wiki/Numbat


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What is the distinction between chemokines, cytokines, interferons and interleukins?
They all seem to describe molecules of similar function and many people seem to use them interchangeably.
Also please include any other similar molecules if I've forgotten any in the list above.

good question!  I'm interested in learning more about chemokines since there appear to be scores of them, many of which must not yet be characterized.

Cytokines is the general class of molecules to which chemokines, interferons, interleukins and others belong. Biologists dispute whether something is a hormone or a cytokine, but generally the consensus goes with if it's to do with immunology it's a cytokine or if the resting concentration is in the picomolar range, but that's a very rough distinction.
Chemokines are molecules that drive cellular chemotaxis. That means they make cells move towards a desired place. Generally chemokines refer to immune cells and there's loads and loads of them.
Interleukins are anything which are messenger molecules between immune cells (inter- means between and -leukins means leukocytes/white blood cells). They're typically denoted by IL + number. However the interferon and tumour necrosis families come under interleukins too in most people's opinion. The interferons are a special group that typically inhibit viruses by making cells non-permissible to viral replication. They also do a few other things like activate macrophages or promote Th1 response, which both also interfere with viruses but there is bacterial overlap. The TNF family is a bit weirder as some are interleukin-like but others aren't as much. TNF-alpha (the classic one) is involved in macrophage maturation. However not all interleukins are strictly between white blood cells, as IL1 acts on the hypothalamus among other leukocytes.
See the problem is everything is a bit grey because most cytokines (if not all) have more than one role and there's never consensus in the world of immunology when it comes to cytokines because more and more keeps getting discovered.

Sounds like immunology in general is just a massive misnomer.

Loads of things in biology were named before they were fully understood. For example haemophilus influenzae doesn't cause influenza - they thought it did before they realised it was a virus. Or the proteins involved in clotting are named numerically 1 through to 12 I think, but don't actually work in order. The immune system has evolved so much from the animal models we use that what we see isn't what we get in the human.

I think 'Junk DNA' is probably a great example of a misnomer ;) but that discussion belongs to chat I suppose XD

In short, this is my understanding following my immunology course (which is mostly identical to AndroidPenguin's answer):

Chemokines: Produce cell movement, i.e. act as chemoattractants. Typically these are used to recruit more immune cells to a site of infection. (Name origin says it all: "chemotactic cytokine = chemokine...)
Cytokines: Produce an inflammatory response by altering transcription (via surface receptor signal cascades). These often act on non-immune cells.

Interferons: A type of cytokine. Secreted by virtually every cell in response to being infected by a virus. Produce an 'anti-viral' state in other cells, through MANY mechanisms. Causes the typical flu-like symptoms.
Tumor necrosis factors (specifically TNF alpha): A type of cytokine. Prepares endothelium (blood vessel walls) to support an inflammatory response by vasodilation, increased adhesion and increased permeability.

Interleukins: Some are chemokines (e.g. secreted by macrophages and dendritic cells upon activation to recruit further phagocytes and adaptive immune cells), others are cytokines (e.g. activating B cells to differentiate into plasma and memory cells after T cell contact).

It should  be noted that not all interleukins yet have a clear function or have an immune-cell source. Also, not all interleukins have an immune-cell target. However, all the ones I know have at least an immune-cell source or an immune-cell target, if not both. Also note that  categories are not mutually exclusive—an interleukin may also be a chemokine, an interferon, or another category not mentioned here like a lymphokine or a monokine.

Pharmacology cross reference: Recombinant type I interferons are injected as therapeutics. Viral infections would seem like logical indications, but interferons are both expensive and have considerable adverse effects, e. g., flu-like symptoms on injection, anemia and depression. Their application is therefore limited to life-threatening viral diseases, e. g. hepatitis C.

Hi welcome to BioStackexchange. Your answer does not exactly address question. Please read the question again and try to improve your answer. Keep contributing !

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Might a previously administered MPSV4 vaccine react with a newly administered MCV-4 vaccine?
This is a hypothetical situation.
Meningococcal polysaccharide vaccine (MPSV4) is a vaccine against Neisseria meningitidis.
MCV4 is a conjugate vaccine.
I would like to know if the polysaccharide base could interact with the conjugate base.
I think they would not act like booster doses and that the efficacy of the conjugate vaccine would be decreased, due to the lifelong effects of MPSV4.
Might MPSV4's polysaccharide base interact with MCV4's conjugate base, and if so, what might be the mechanism?


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Is it possible to sequence only the 16S rRNA component? If so, how?
There have recently been several papers on using 16S rRNA as a way of identifying species (here, and here). I'm wondering if it's possible to sequence either just that subunit of the ribosome or just the sequence of DNA that it comes from (probably not, I know). That way you can use only the sequence you need to compare against other 16S rRNA sequences to test for novel species.
If so, what is the process involved?

Maybe I am just over-reading your question, but why would you think sequencing 16S would be more complicated that sequencing any other gene?

Well I think that the simple answer is yes and in fact it is commonly done.

@nico & bobthejoe well I'm unfamiliar with the process of sequencing genes, so I don't have any idea of how it's done. Could you explain the process? I'll edit the question.

you should probably just read about colony PCR.  that is the simplest method...

Basically, all 16S genes are highly conserved, i.e., they share much identical bases. This means one can bind the 16S gene piece (after DNA was cut) to a specific other piece of DNA, even if you don't know exactly the 16S gene bases. Everything else is discarded then. Now finally, using PCR the rest is amplified and sequenced. Sequencing 16S only is much less work, so that's how they did it years ago. Today, whole microbiomes are sequenced by professional labs.

Is it possible to look at the actual rRNA molecule and get the sequence of rRNA rather than sequencing the DNA the encodes for it?

I don't know but I think it would make a good question. 8)


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Do antibiotics attenuate immune response on subsequent exposure to same bacteria?
A healthy immune response to a bacterial infection includes "memory" to permit the body to thwart subsequent exposure to same bacteria.  What are the dynamics of using antibiotics on initial exposure to the bacteria regarding a possible degradation of the quality of this "memory" and thus the body's possibly compromised ability to fight a repeat exposure to same bacteria ?
I am not speaking of vaccines ... focus here is on bacteria

A quick search on ISI Web of Knowledge yielded this paper:

R J North, P A Berche and M F Newborg (1981) Immunologic consequences of antibiotic-induced abridgement of bacterial infection: effect on generation and loss of protective T cells and level of immunologic memory. Journal of Immunology 127: 342-346

The authors investigated the effects of ampicillin treatement in mice infected with Listeria monocytogenes. They reported an abridgement of T cell-mediated antibacterial immunity and in particular an effect upon the development of memory:

Moreover, Ampicillin-induced abridgement of infection, either before or at the time of peak primary response, resulted in the expression of greatly reduced levels of immunologic memory at a later time. This indicates that memory cells are generated throughout the entire course of the primary anti-Listeria response, including the period of its decay.

Presumably any treatment that reduces the need for an immune response will have an effect upon the production of useful memory T cells.

It is also conceivable that the increased presence of the interior (cytosol) and cell wall parts of dead or dying bacteria will cause an enlarged adapted immunity response. I remember that EHEC patients were specifically not treated with antibiotics from fear of freeing more toxins from dead bacteria.

Edited for Clarity:
In order to invoke a memory response or create a memory response, there must be interaction with the Adaptive Immune System (usually CD40+ "Helper" T-Cells), and the interaction must come in the form of a protein since the MHC receptors only respond to proteins.
Antibiotics are usually smaller macromolecules that directly cause slower growth or kill the microbe. They will *not* create or illicit a memory response because they are not presented to the immune system to initiate the proper procedure, and may not be proteins and unable to be presented in the first place.
If you're asking about vaccines (which was my inference before the edit), then they stimulate what is basically the same memory creation mechanisms that normal infections do. Antibody counterparts recognized by B-Cells are paired with proteins from the disease you want to immunize against, called the Hapten and Carrier respectively. Then the protein is processed via the B-Cells, presented to T-Cells, and a memory response is made.
My apologies if the previous answer was more ambiguous.

I am sorry, but are you talking about antibiotics or rather vaccines?

Ah, good point. I think my answer had more to do with vaccines. I'll clarify it.

@MCM That makes a lot more sense, reversed my downvote.  I think the OP (and myself) was also interested in whether there is a reduced production of memory cells in an infection treated with antibiotics rather than one that was not (as opposed to a memory of the antibiotic itself).

For Antibiotics, I'm not aware of any change in the Adaptive response. Some vaccines don't have quite the same long-lasting memory response as having to fend off the infection naturally (though I've not been explained why), but can still last for years or decades. If someone else is more aware than I am, feel free to answer - I've only taken the basic courses thus far.

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Is brain plasticity such that we can train ourself to see with our ears?
I am finishing writing some code which will parse a photo (eventually video) and use all the RGB information to synthesize an audio representation. I am wondering whether a typical person has sufficient neural plasticity to learn how to listen to this audio to understand an image in a general sense? I am not looking for perfection.  If the person has good vision they would do well to spend time listening to such synthesized audio while simultaneously viewing reality to give some training to enhance their interpretative abilities.  Once trained they could augment or supplant vision with its sonic equivalent.

How plastic is our audio-visual brain? Is there hope this will work ?

PS.  Once working I will update this Q

For those wondering about the details :  I am traversing the image using a Hilbert Curve which tends to preserve spacial relations amongst pixels to minimize re-training upon change to pixel resolution.  This flattens the 2D photo into a 1D line sprinkled across from left to right with points storing respective pixel values (at a 1st approximation I collapse RGB into grayscale 0.21 R + 0.72 G + 0.07 B)
... to create the audio representation I visit each pixel position on this line and introduce an audio frequency oscillator per pixel at a unique frequency such that the beginning pixel at far left is given the lowest frequency in our range (say 200 hertz) on upward until the oscillator frequency at the far right pixel renders the highest frequency (say 10 khz) ... the grayscale value drives the volume of that pixel's oscillator
... further details at:  isomorphism between video and audio
                https://www.youtube.com/watch?v=DuiryHHTrjU
Beauty of this approach is it lends itself to performing this transformation in reverse (a bijection) - from audio to video we can use a Fourier analysis ( FFT ) of audio mapped into pixels - then back again to audio, rinse and repeat ...

Please send in some sounds for the mapped images!!!

Short answer
Yes, we can see with our ears.
Background
Bach-y-Rita famously stated "We see with our brains, not our eyes". Bach-y-Rita worked for decades on sensory substitution. Sensory substitution approaches in general aim to replace for a lost sense by redirecting information normally captured by that sense to another still functional one.
Bach-y-Rita focused on substituting vision by tactile information. His Tactile Vision Substitution System (TVSS) captured camera images and translated them to tactile images projected onto the back of blind subjects. His decades of research eventually culminated in the commercially available BrainPort device (Stronks, 2016).
Vision-to-auditory substitution devices have also been developed, most notably the vOICe by Peter Meijer and the prosthesis-substituting-vision-by-audition (PSVA) device, among others. The vOICe translates images into sounds by re-mapping their x-axis into the time domain, and their y-axis into the frequency domain (Meijer, 1992). This “image-sweepline” technique has subsequently been deployed in the EyeMusic device for use in sensory substitution (Abboud et al., 2014). The PSVA makes use of a pixel-by-pixel acoustic frequency transformation,where vertical position is coded as pitch and horizontal position as binaural intensity and phase differences, and brightness into loudness (Capelle et al., 1998).
Peter Meijer refers to the vOICe as generating 'soundscapes', much like the approach you are describing. I seriously encourage you to contact him, he is a very nice guy and open to exchange.
Anyway, to come to your question - can we see with our ears? Yes we can. Several studies have indicated that sounds can successfully be used to perform visual tasks, including localization (De Volder et al., 1999), pattern recognition (Arno et al.,2001a, 2001b) and depth-perception (Renier and DeVolder, 2010).
Several studies have shown that the visually deprived brain is capable of re-routing auditory sensations into visual equivalents by re-routing this information to the de-afferented visual cortex in the blind (reviewed in, e.g., Poirier et al., 2007). This is referred to as cross-modal plasticity of the brain.
However, the learning curve is quite steep, in that a lot of practice is needed to obtain useful information from visual information coded through sound (Stronks et al, 2015). Further, what is probably the biggest issue in analyzing soundscapes is visual clutter. While the visual system is very well capable of filtering out image clutter and extract the useful information, soundscapes will inevitably turn every irrelevant object in the scene into a corresponding sound. Front-end visual processing techniques are likely to be key to turning an auditory visual substitution device into a practically feasible device for the blind, or the sighted for that matter.
The visual cortex is recruited for auditory tasks in the blind, but not in the sighted. However, I am inclined to believe it is practice, and not visual deprivation per se, that determines the performance with sensory substitution approaches in general (Stronks et al, 2015).
References
- Abboud et al., Rest Neurol Neurosci (2014); 32: 247–57
- Arno et al., Neuroimage (2001a); 13(4): 632–45
- Arno et al., App Cog Psych (2001b); 15(5): 509–19
- Capelle et al., IEEE Trans Biomed Eng (1998); 45(10): 1279 - 93
- De Volder et al., Brain Res (1999); 826(1): 128–34
- Meijer, IEEE Trans Biomed Eng (1992); 39: 112–21
- Poirier et al., Neurosci Biobehav Rev (2007); 31(7): 1064–70
- Renier and De Volder, J Integr Neurosci (2010); 4(4): 489
- Stronks et al., Brain Res (2015); 1624: 140–52
- Stronks et al., Expert Rev Med Dev (2016); 13(10): 919-31

If a lot of practice is needed to obtain useful information, than the learning curve is quite shallow, rather than steep (that increase in learning doesn't happen until you've moved a long ways along the x axis and put a great deal of practice in). But this is a wonderful answer on a very interesting subject all the same :)

@DeNovo yes the meaning of a steep learning curve is often used as it is used here, but honestly I've always wondered why it is used often in the sense that 'much learning is needed'. I'll think of improving my answer. Thanks

I would like to add to the great answer by AliceD with my own experiment.  I wish to add this because the results, while intellectually natural, were intuitively fascinating, and because my sample size is tiny (read: N=1), and I'd love to have others go out and repeat the experiment.
I don't quite show that you can see with your ears, but I do think it shows that you can hear with your eyes.  (Or, more formally, we fuse our senses in a remarkable way)
The bill of materials is daunting:

Two spoons
Willing test subject

In my case, the subject was my girlfriend at the time.
It is known that we use spectral effects to determine the elevation angle of a sound.  Our ears and our shoulders are known to shape the sound, emphasizing some frequencies and muting others.  Of course, this process is impossible to do if you don't know what the sound was "originally."  If you don't know what the sound was as it reached you, you can't figure out how much the ears have colored it.
For this experiment I picked two spoons, and verbally described what I was going to do.  I was going to click the spoons in various places and have her reach for them.  I intentionally did not click the spoons together in this demonstration because I did not want her to get to hear the spoons until the experiment started.
I first asked her to close her eyes.  I clicked the spoons in various places, and she identified which direction she thought it came from.  She was reliably accurate in left/right direction, because she could hear the time delays between the sound hitting her left and right ear.  However, her elevation angle was rather random.  There did not appear to be any pattern at all to it.
Then I asked her to open her eyes, and do a very boring version of this experiment.  With her eyes open, she of course was able to point to the clicking spoons 100% of the time.  (This was actually the hardest part, because it seems absurd to the test subject.  They start to think it's a trick).
Then, I had her close her eyes again, and repeat the experiment.  The results?  She was dead on every time.  Didn't miss a single one, both azimuth and elevation.
So what do I claim happened?  When we started the experiment, she did not know the frequency spectra of the spoons clicking.  As such, she could not effectively back out what transform her ears and shoulders were applying, and could not figure out elevation angles.  She could make some guesses, as a human that has heard things clacking together, but that was insufficient to accomplish the task.
In the boring second phase, she could now fuse the information she got from her eyes in with that from her ears.  Now she could determine what angle the sound was coming from with her eyes, figure out what the transform of her ears/shoulders should be, and back out what the "true" sound of the spoons was.
In the third phase, she now knew the "true" sound of the spoons, so whenever soundwaves hit her ears, she could use that knowledge to figure out what transform her ears/shoulders must have been applying, and figure out angles.
I used this to argue that we can hear with our eyes, but it might be more effective to say that the brain doesn't pay as much attention to the division between the 5 senses as we do when we talk about our sensory experience.  As far as it is concerned, it's all simply neural stimuli.  It will fuse these into one coherent image, and that is what really matters.

+1, but the anecdotal report, while making an interesting read, is not too convincing as no one can verify your findings and their validity. Could you add sources of any kind?


text:
What does "thermodynamic equilibrium" mean for an enzyme-substrate complex?
From Fersht, Enzyme Structure and Mechanism p. 87:

The Michaelis-Menten mechanism assumes that the enzyme-substrate
  complex is in thermodynamic equilibrium with free enzyme and
  substrate.

In my understanding what this means is that the (E-, S- and ES-concentration dependent) rates of association and dissociation have equated.
So we're kind of in this situation:

where "product" would be referring to [ES] and "reactant" to [E] and [S]. Does that make sense?

Product is still $P$; $ES$ is the transient Enzyme-Substrate complex. If you mean product in the sense of product of a reaction then yes but it is a confusing usage. So stick to calling $ES$ as a transient state

@tmottm Can you please accept answers, which answer your question satisfactory? This is a nice gesture towards the people who write the answers. You can find all your questions in your User menu.

Thermodynamic equilibrium means that:
Rate of forward reaction = Rate of backward reaction
In this case:
$E + S\xrightleftharpoons[k2]{k1} ES\\ \ \\
 \ \\ \\ at\ equilibrium:\\ \  \ \\ \ k1.[E][S] \tiny{\ (forward\ rate)}\normalsize=  k2.[ES] \tiny\ (backward\ rate)
$
This was the initial assumption in the Michaelis-Menten model.
Later on this was improvised by assuming pseudo-steady state of ES complex. This means that $[ES]$ does not change over time, which is both as a result of its production by the reversible reaction:  $E + S \leftrightharpoons\ ES$ and consumption by the irreversible reaction $\ ES\ \xrightarrow{k3} E+P$
that is:
$k1[E][S]\tiny\ (production)\normalsize=(k2+k3)[ES]\tiny\ (consumption)$


text:
Does Darwin's Theory of Evolution refute Terence McKenna theory "Stoned Ape" theory of human evolution?
I haven't read it but I'm asking for a quick answer.
As far as I know, Terence McKenna's theory of evolution in humans main concept is that a hominid has tried in their diet psilocybin mushrooms, and the experience they integrated changed their mind in a way that led to "us."

to call it a theory is seriously stretching the term. it barely qualifies as a hypothesis.

@user1136 I know of no paleontologist working on hominids who takes it seriously, it sets out to explain something that does not need explaining and does so with bad outdated psychology and just so stories. Worse it ascribes behaviors as unique to humans that we no are not, and that non existent uniqueness is what it pretends to explain.  It is not based on any paleontological evidence, and even the author of the study it cites for the effects the mushroom criticize it for grossly misreading the effects of said mushrooms.

How can one theory refute another theory? And you haven’t read it? And nobody has removed this in seven years! Let’s do it!

Briefly the "Stoned Ape theory" posits that psychoactive Psilocybin mushrooms in the diet of pre-Homo sapiens primates catalyzed the change Homo sapiens.  It suggests that the mushrooms conveyed selective benefits to consumers of the mushrooms, dissolving the 'egos' of our ancestors and allowing them to form communities.  It may also be sexual stimulant, goes the theory and so may have conveyed an advantage there.
I think this theory is not terribly popular now, but it is difficult to refute or to prove.  The only real proof would be to take a hominid or any other species and give them the fungus and see if they become intelligent.   Just because this has not happened does not disprove the theory.  the only other way to prove this really would be to have a time scope and look back and see what happened.  Its a similar question as to how life emerged on Earth.  We have some interesting evidence but conclusive proof is going to be hard to get.
I found a large collection of supporting evidence.  Even the definition of human intelligence and whether it is so unique is subject to debate.  Certainly there are other primates who appear to be as or more social than we.  I think other theories seem as or more likely.
Darwin's theory of evolution doesn't refute many theories of how something happens in evolutionary history.  The Panspermia hypothesis is taken quite seriously at this point - could it be that life originated elsewhere then was introduced here by meteorites.  The origin of Species doesn't have a lot to say about that.  I think the same is true for the emergence of human intelligence, which at this point we believe is unique on Earth.  Hard to make an irrefutable theory based upon a single example.

its fairly easy to refute, since the author of paper it cites on the effects of mushrooms has criticized it for completely misinterpreting the effects, and the timeline it predicts as well as the changes it posits do match the paleontological record. its refuted for the same reason a theory that humans coevolved with wolves 8 millions years ago is refuted, it doesn't match the fossil record in the slightest, regardless of the reasoning.

Refute?  No.
Shigeta summarized the work pretty well, and though I have my own opinions on McKenna's theory the fact is that Darwin and McKenna are not opposed.  The "Stoned Ape theory" is a specific idea for how human intelligence might have appeared from earlier hominids.  Darwin (and Wallace) proposed a broad theory that has borne out for the process of evolution by natural selection.  Evolution applies to populations large and small, whether human, primate, or bacterial.
Evolution, however, is not particularly predictive and would say nothing about what might happen should some primates eat some entheogens.  McKenna's idea could fit into reality, although as Shigeta said it is difficult to prove, but there is technically no Darwinian reason why it couldn't have happened.  Darwin did write about human evolution in The Descent of Man.

a belated thanks for the props... - 8 years later...lol

The stoned ape "theory" ("we owe our very existence as a species to psychedelics") isn't theory, despite it's pretense. There is no support for it in evidence, or in theory. Nor can there be because in its own terms it defies both. It's founder seems to have thought himself a genius, and solicited a cult-like following determined to spread his message, as their own. He had no college-level science education - see facts and citations below (*).
Bear in mind the "theorist's" target audience when he wrote Food of the Gods. Not scientists nor anyone scientifically literate. In his own words: "[The target audience is] the 18-25 year old group that is drug-friendly but has no rationale except that it's a good time" (Gracie, Zarkov & McKenna interview).
As for his understanding of evolution, the scope of his grasp, here's what he thought science says - if you believe what he says. No harm to have smelling salts in easy reach if you're minimally educated in biology, i.e. high school level:
"Conventional evolutionary theory tells us that small adaptive changes eventually become genetically scripted into the species" (OMNI interview)
Obviously that's 180 degrees backward from true or accurate, a recitation of what Lamarck thought - over 200 years ago, and before anyone ever heard of Darwin, or natural selection.
There's nothing theoretical in the "stoned apes" storyline, despite its claim. It's not a theory, its malarkey of the same type as Creationism - but from the opposite fringe: new age psychedelia, not old time religion.
(rolls eyeballs)
*TM was at quite a disadvantage for science ed. For any major in college, even liberal arts - there's normally a 'general studies' science requirement. Its a minimal basic in higher ed, across the board. But TM's college program (Tussman Experimental) is one that specifically, uniquely excluded science. And short-lived as it was, the college was roundly criticized in its day on that very point. Its founder made excuses, e.g. this quote (from Tussman's book EXPERIMENT AT BERKELEY):
"It is recognized that the program does nothing in the way of integrating science with the social sciences and humanities. We leave this two-culture problem for wiser men to solve. In this respect, however, our students are either better OR WORSE OFF than others" (caps added for emphasis).
Obviously lame? Colleagues in education didn't buy it. For example, this remark from Sidney Rosen (Univ of Illinois): "By his admission that he cannot find a way of integrating scientific ideas into a basic two-year program, Mr. Tussman is guilty of contradicting the educational goals he defends ... It is difficult for me to see how the curriculum can flourish without science as an integral part." - Journal of Research in Science Teaching 7: 271 (1970)
Prescient? The college didn't flourish, it floundered. It was already crashing when Rosen wrote that. In fact, the 'experiment' seems to have perhaps been a case of politics in education, masquerading as 'educational reform.' TM himself offers an interesting remark along just such lines:
"... it was an experimental program... this thing called the Tussman Experimental College. I arrived at Berkeley the year after the Free Speech Movement ... in an effort to keep the place from blowing sky high they had told this left-wing professor that he could have an experimental section of the university" (www.tripzine.com/listing.php?id=terence1)
This is the kind of info those who think they're all into McKenna, all about his rap and 'ideas' - have no clue.  Zero, none.  Knowing anything whatsoever, that's able to be factually established, double-checked and verified as true and accurate, valid - ain't its ticket.

Hi, whilst I wasn't involved in the original editing of your answer please be aware that the Stack Exchange model allows anyone to submit edits for peer review.  Please refer to this page for further help.

Thank you for the page link.  After reading it along with your comment, I can only conclude the policy you cite - as explained - is critically unclear and suborns tampering with posts, such as has happened with mine.  Thanks to your page link, I see five criteria specified for edits.  And I find that what was done with my post - violated not one, or two of them - but all five:

The other answers have done excellent job explaining how the stoned ape theory contradicts the Darwin's own theory of human origins. What remained unmentioned is that Darwinism have been the basis of the modern evolutionary theories for more than a century, and in this modern light there are even more glaring contradictions between the McKenna's theory and the reality.
More specifically, there is little to support this theory from the point of view of molecular and population genetics. One could imagine two scenarious here:

Consumption of the psychoactive mushrooms was a single event that triggered a germline mutation in the most-recent common anscestor of the modern homo sapience (pretty much in the same way as cancerous mutations are known to be triggered by exposure to toxic substances). Note that this scenario, tracing our ancestry to a single mutant, already contradicts the McKenna's picture of a mushroom consuming prehistoric culture. Moreover, divergence of species requires more than a single mutation, and it is improbable that multiple beneficial mutations could have arisen this way.
The psychoactive mushrooms could have been a part of the diet of homo erectus throghout hundreds of thousands of years - sufficient time for accumulating enough mutations to evolve into a separate species. While these mutations could make humans more adapted to surviving while being stoned, they are no replacement for mushrooms. In other words, the effect of mushrooms would disappear once their use was discontinued, leaving a species with a doubtful benefit of adapted to survival while being stoned (any evidence that drunk or stoned people are less likely to harm themselves in dangerous situations is at best anecdotal).

Let us finally note that McKenna's time scale for homo sapience diverging from homo erectus (100,000 BCE) is at odds with the established paleontological scales. In fact, it even post-dates the humans common ancestor with Neanderthals and Denisova people (about half a million years ago), which is attested on genetic level for both neandertals and densova people.

@user1136 I think that the only way it may not contradict the modern synthesis is, if we assume that homo sapiens had already existed as a species capable of consciousness, and the mushrooms only served to wake this consciousness. This is even more so for language, since it requires specific physiological particularities, which many apes simply do not possess.

@user1136 I don't know that there are many, if any, serious neuroscientists who would claim consciousness is in any way unique to humans. There is no gap.


text:
What is the recommended PPM when foliar feeding L-amino acids
It is said that L-amino acids such as histidine, methionine, aspartic acid, glutamic acid, asparagine and glutamine can revert plant stomata closure, increase quality of fruits and assist maturity. It is also said that the best way to apply is through foliar feeding.
I would like to start experimenting with different amino acid foliar feeds but would first like to know if there is a recommended maximum/minimum/recomended Parts per million(PPM) , for foliar feeding of these compounds.

I know that some of the amino acids you listed are commonly found in fish fertilizer. I haven't read any studies on the use of these amino acids individually and not sure where you would purchase them separately. If you're just experimenting in your own garden I would just use fish fertilizer according to the label directions. If you look for fish fertilizer studies you'll probably find more info.
Also, I've never heard of these opening up the stomata of the plants. The only references I've read indicate that foliar sprays are best applied in the early morning or late day when the stomata is already open. This is how the nutrients get absorbed from the leaves.
I don't know that I would want to intentionally manipulate stomata closure. The plant knows when it needs to breath.
Where did you read the above info? I'd be interested in seeing it.

From my understanding stomata close when light and humidity are low, and temperature and salt concentration are high. When stomata close, photosynthesis and nutrient absorption slow and the plants respiration is increased. this slows plant growth and can affect end of year yield applying L-aminos favours the opening of stomata and increases plant health and growth in adverse conditions. Body builder shops stock individual l form aminos that are easily dissolved in water thus my ppm question.


text:
Criteria for the numbering of human chromosomes
What were the criteria devised for the numbering convention employed in human chromosomes? When was it fixed?
Correct me if I am wrong; it appears that chromosome pairs 1 to 22 were originally ordered in terms of perceived structural size, which ended up fitting neatly with the quantity of base pairs (but not with the quantity of genes).
The sex chromosomes in turn were arbitrarily assigned as "pair 23".
Is this sound?
Thanks in advance.

Why do you think it was "fixed?"  Here's a nice review of the history of human cytogenetics, which included not only the original image from 1956 but points out a report which comments on the standardization of chromosome number.  The autosomes were indeed numbered by length, and the sex chromosomes are traditionally put at the end as they are "numbered" 23 but clearly function quite differently.  Gene content was decades away from being known at the time, and honestly isn't even known now.  It's also just as arbitrary; simple size is easy enough and makes for rather nice pictures.


text:
How does hemoglobin-free blood transport oxygen?
Snails... We have some kind of huge garden snails appearing lately (read since the last 10 years or so). Try as one might, it's impossible to avoid them when driving. These snails do not appear to have red blood - I doubt they have blood at all. Wikipedia tells me blood's red colour is due to haemoglobin - which serves to transport oxygen.
How do snails (and any other animals that do not have red coloured blood) get oxygen? Or, do such animals need no oxygen at all?

Snails, like most molluscs, have a protein called hemocyanin dissolved directly in the hemolymph ("blood"). Hemocyanins are copper-containing metalloproteins: the binding site for a single O2 molecule contains two copper atoms. Unlike hemoglobin, where reversible oxygen binding is accomplished without a change in the oxidation state of the Fe(II) atoms in the heme prosthetic groups, in hemocyanin the copper undergoes a transition from colourless Cu(I) in the deoxygenated state to blue Cu(II) when oxygenated.
Incidentally, there are certain species of fish that manage with little or no hemoglobin - icefish.


text:
Which enzyme catalyzes transcription and which translation?
My attempt:
Transcription - RNA polymerase
Translation - aminoacyl tRNA synthetase
I know that the ribosome almost runs translation, but I don't think ribosomes are enzymes, which is why I went with aminoacyl tRNA synthetase.  Is this right?

Depending on how specific you want your answers, you should define which steps you want the enzymes for. Transcription uses several enzymes, and Translation the same - including Ribozyme activity at the aminotransfer site in the Ribosome.

This would be a great time to look up what the 2009 nobel prize was awarded for.


text:
Anti-parallel DNA code operons
Coming from a software engineering standpoint, suppose I have a string of code like so:
... 5'-ATAGAC-3' ...
... 3'-TATCTG-5' ...
Assume the above code is part of a larger segment. Now, reading from 3' to 5', the promoter and operator would be somewhere before the structural gene on the 2nd stand:
(Promoter) (Operator) ... 3'-TATCTG-5' ...
Where would it be on the first strand? From what it looks like, the first strand codes for a completely different protein than the second stand:
... 5'-ATAGAC-3' ... (Operator) (Promoter)
Yet, the two strands are complementary.

You make one mistake: DNA is always read in 5'->3' direction. So when you promoter is before the gene, it is on its 5' site. So it would be 3'-TATCTG-retomorp-5' or in the right reading direction: 5'promoter-GTCTAT-3'.

related: http://biology.stackexchange.com/questions/14299/on-which-strand-does-the-promoter-sit

DNA is built 5'-3' but the template strand is read 3'-5'.

In your example, yes the two strands do code for different proteins. However, biologically this generally doesn't occur. I say generally because I don't want to rule it out definitively but I don't know of an instance where both strands at a given locus code for a protein and, where it does occur, it is often used as a criterion for annotating one of the elements as dubious. Along with that, there would be no promoter immediately 5' to one of the strands. Even if it does occur biologically, each strand would code for a different protein and would be a different gene.
In any gene, one of the strands is identical to the RNA transcript (before processing and with T instead of U). This is called the coding or sense strand and runs 5' -> 3'. The other strand is used as a template by RNA polymerase (RNAP) to polymerize the RNA transcript. It runs 3' -> 5' and is called the template or antisense strand.
Also, a note on promoters: promoter consensus sequences by convention are given on the sense strand. However, as far as I know, transcription initiation factors recognize the base pairing between both strands in the major groove of dsDNA because they must bind before promoter melting occurs. Thus, I wouldn't say that a promoter exists only on the template strand.

So would both DNA stands code for the same protein at a given locus? How is this possible, given that the bases are different when reading one strand vs. the other?

No, they would code for two different proteins and in opposite directions…

Thanks. How does the cell "know" which strand to read? What I mean is, you mentioned that "transcription initiation factors recognize the base pairing between both strands in the major groove of dsDNA". How does it know which strand to read? The promoter strand?

The strand is determined by the promoter location. Since promoters are directional and transcripts are only polymerized 5' -> 3', there is only one choice for sense and antisense strands from a given promoter.


text:
Are antibodies and hepatitis viruses of similar adaptability?
Antibodies and Hepatitis viruses both have hypervariable regions.
Is one more adaptable than the other?
Precisely how adaptable are they?
I have read that antibodies can be trained to bind to almost any antigen, is the same true for Hepatitis?
Long-Term Evolution of the Hypervariable Region of Hepatitis C Virus in a Common-Source-Infected Cohort
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC110045/
I guess the first step to answering this is to find/conduct a study in which the Hepatitus virus is mutated and selected for a particular antigen. I am not sure if this has been done, but it definately has been done for antibodies.

Can you please add some references for the variable region of the hepatitis virus?

My initial thought is that this question is either too opinion-based or too broad, the comparison between members of different categories, and the measure of "how adaptable" is non-specific and environment-dependent.

@BryanKrause Can It be trained to attach to a particular antigen? how adaptable means how many antigens can it be trained to identify.

First off, you probably mean antibody-producing cells; a given antibody can't be trained or adapted, it's just a protein, and it will bind whatever fits in its antigen-binding region. I don't think it's really reasonable to count the number of antigens, because there doesn't necessarily have to be a one-to-one ratio: a given structure can potentially bind many different antigens, as long as there exists an appropriate motif that "fits."


text:
Knockout Rat Phenotype Database?
Is there a database where I might list the phenotype of a certain rat knockout and/or search for other similar phenotypes?
There is a International Mouse Phenotyping Consortium, which has the goal of characterizing the phenotypical changes of homozygous knockouts for each of the 20,000 genes in the isogenic mouse line C57BL/6.  The International Knockout Mouse Consortium is responsible for creating the knockouts and the two consortiums work together closely.
There is also a Knockout Rat Consortium, but I haven't found a Phenotype Change database for rats.

Opinion:
the Jackson laboratory
http://jaxmice.jax.org/
Is the industry leader in transgenic mouse production. Their list of mouse strains is almost a db in itself but currently no db exists that I'm aware of. I take it your looking for something similar to what's available for c elegans:
http://www.celeganskoconsortium.omrf.org/


text:
Is ebola non-contagious until symptoms appear? Why?
There's been a lot of talk lately about the man who recently came down with ebola in Dallas, Texas. While I live elsewhere, I keep hearing quotes from CDC and state officials that ebola is not contagious until a person shows symptoms. This is generally used in the context of "Don't worry too much; we have the situation under control." Is this true in all cases? Why?

Every infectous disease works this way: if you had contact with x particles (virus, bacteria, etc...), then you have y% chance to get infected (depends on your immune system, luck, etc...), so it has a distribution. This is called virulence, and it can be measured with ID50 (infectious dose by 50% of subjects) and LD50 (lethal dose by 50% of subjects) values. According to animal studies the LD50 is very low by ebola, so it is highly virulent, but it highly depends on the mode of transmission. So this virulency is compensated by low transmissibility: people infected with ebola, but not showing symptoms release too small amount (or nothing) of the virus to infect others. By hemorrhagic fever you bleed out of every hole of your body, and that blood contains a lot of viruses, that's when it can infect others. So this is not a "Don't worry too much; we have the situation under control." case, it works this way currently. This can probably change due to mutations.

Symptoms usually begin with a sudden influenza-like stage
  characterized by feeling tired, fever, pain in the muscles and joints,
  headache, and sore throat.1[12][13] The fever is usually greater
  than 38.3 °C (100.9 °F).[14]
This is often followed by: vomiting, diarrhea and abdominal pain.[13]
  Shortness of breath and chest pain may occur next along with swelling,
  headaches and confusion.[13] In about half of cases the skin may
  develop a maculopapular rash (a flat red area covered with small
  bumps).[14]
In some cases, internal and external bleeding may occur.1 This
  typically begins five to seven days after first symptoms.[15] All
  people show some decreased blood clotting.[14] Bleeding from mucous
  membranes or from sites of needle punctures is reported in 40–50% of
  cases.[16] This may result in the vomiting of blood, coughing up of
  blood, or blood in stool.[17] Bleeding into the skin may create
  petechiae, purpura, ecchymoses, or hematomas (especially around needle
  injection sites).[18] There may also be bleeding into the whites of
  the eyes. Heavy bleeding is uncommon and if it occurs is usually
  within the gastrointestinal tract.[14][19]
Recovery may begin between 7 and 14 days after the start of
  symptoms.[13] Death, if it occurs, is typically 6 to 16 days from the
  start of symptoms and is often due to low blood pressure from fluid
  loss.2 In general, the development of bleeding often indicates a
  worse outcome and this blood loss can result in death.[12] People are
  often in a coma near the end of life.[13] Those who survive often have
  ongoing muscle and joint pain, liver inflammation, and decreased
  hearing among other difficulties.[13]
The time between exposure to the virus and the development of symptoms
  of the disease is usually 2 to 21 days.1[10] Estimates based on
  mathematical models predict that around 5% of cases may take greater
  than 21 days to develop.[11]

wikipedia - Ebola virus disease

The LD50 of mouse-adapted EBO-Z virus inoculated into the peritoneal
  cavity was ~1 virion. Mice were resistant to large doses of the same
  virus inoculated subcutaneously, intradermally, or intramuscularly.
  Mice injected peripherally with mouse-adapted or intraperitoneally
  with non-adapted EBO-Z virus resisted subsequent challenge with
  mouse-adapted virus.

1998 - A Mouse Model for Evaluation of Prophylaxis and Therapy of Ebola Hemorrhagic Fever

Although outbreaks of Ebola virus have largely been confined to
  endemic regions, their high fatality rate, ability to transmit
  person-to-person, and low lethal infectious dose make Ebola virus a
  dangerous threat to public health and pose a great risk for
  researchers working with these viruses as well as health care
  personnel treating patients during outbreaks. Furthermore, their
  potential to be developed into aerosolized biological weapons also
  causes grave concern for their use as a bioterrorism agent ( Bray,
  2003).

2008 - Protection against lethal challenge by Ebola virus-like particles produced in insect cells

Some interesting story about the topic (others were not so lucky):

In 2004, a virologist at USAMRIID was working in a BSL-4 laboratory
  with mice that had been infected 2 days before with a mouse-adapted
  variant of the Zaire species of Ebola virus (ZEBOV) (2). The virulence
  and infectious dose of this variant of ZEBOV are unknown in humans;
  wild-type virus has a case-fatality rate of up to 90% (3).
The person had been following standard procedure, holding the mice
  while injecting them intraperitoneally with an immune globulin
  preparation. While the person was injecting the fifth mouse with a
  hypodermic syringe that had been used on previous mice, the animal
  kicked the syringe, causing the needle to pierce the person’s
  left-hand gloves, resulting in a small laceration. The virologist
  immediately squeezed the site to force the extravasation of blood.
  After decontamination of the blue suit in the chemical shower, the
  injured site was irrigated with 1 liter of sterile water and then
  scrubbed with povidone-iodine for 10 minutes.
In terms of exposure risk, the needle was presumed to be contaminated
  with virus-laden blood, although it was suspected that low levels of
  virus were present on the needle. The animals had not yet manifested
  signs of infection, and much contamination may have been removed
  mechanically when the needle pierced the gloves. The local
  decontamination of the site also reduced potential for infection.
USAMRIID medical, scientific, and executive staff concluded that the
  person with potential exposure warranted quarantine in the MCS.
  Contact plus airborne precautions (gown, gloves, N95 mask, eye
  protection) were used, with a plan to upgrade to BSL-4 precautions for
  signs or symptoms of illness. These extra precautions were instituted
  while the patient was asymptomatic for several reasons: 1) the timing
  of initial clinical manifestations with regard to potential for
  shedding virus were not known for this specific isolate in human
  infection; 2) there was interest in ensuring all infection control
  procedures were being followed appropriately in advance of clinical
  illness; and 3) there was interest in reducing any potential
  confounders, such as a caregiver transmitting a febrile respiratory
  infection to the patient, which might lead to unnecessary procedures
  or additional isolation. The person was monitored for routine vital
  signs; daily laboratory studies (coagulation studies, blood counts,
  chemistries, viral isolation, D-dimer) and regular physician
  assessments were performed.
Over the next several days, discussions were held with several
  internationally recognized filovirus experts regarding potential
  treatments or postexposure prophylaxis options. Local and state public
  health officials were also notified. The consensus opinion was that
  there was no safe, readily available source of immune plasma and
  little evidence existed to support its use. Emergency investigational
  new drug (IND) protocols were established for treatment with
  recombinant nematode protein (rNAPc2) and antisense oligomers, with
  the intention to consider implementation only if the patient
  demonstrated evidence of infection.
Ultimately, none of the 5 mice had confirmed viremia at the time of
  the incident. The patient did not become ill or seroconvert and was
  discharged after 21 days.

2008 - Managing Potential Laboratory Exposure to Ebola Virus by Using a Patient Biocontainment Care Unit


text:
Why are bees eating the wax?
I left outside a piece of wax few weeks ago and each day I saw lots of bees "eating" it. Why do they do this when they can create new wax? (it seems a really hard work considering how little was taken in the course of few weeks).

I do not have an answer but it is a very cool observation and photo; thanks for posting it.

Recycling?  One would think that it's more efficient to re-use old wax than to make new.  Was your wax beeswax, or something else?

@jamesqf It is fully natural beeswax that I solar melted from their old combs. I use it to seal tree cuts.

It's unclear how costly wax production really is, here are a few resources with some guestimates and studies:
http://www.honeybeeworld.com/diary/articles/fdnvsdrawn.htm
http://www.beesource.com/forums/archive/index.php/t-260700.html
http://www.bushfarms.com/beesharvest.htm#expenseofwax
But doubtless wax is costly to make. So it seems totally reasonable that your bees are actually collecting wax. But my guess, if they were doing this in October, is they drawn by the smell and were poking around for something besides wax per se, like sugar or pollen bits in the wax.
I just saw honey bees buzzing around a compost pile on a warm day in January, focusing on orange peels and used coffee grounds. They would masticate both grounds and peels with their mandibles, but to my eyes weren't actually collecting anything (they didn't bring it to their mouths with their tongues nor pack anything on their corbiciculae). I suspect they will pick at lots of things when there's not a strong pollen or nectar flow, maybe for medicinal reasons or the like, or perhaps more "for something to do."


text:
Why do gram-negative bacteria attack the digestive system more than gram-positive ones?
I was researching for a biology project on the subject of contagious infections of the digestive system (mainly the intestines) and almost all of the bacteria that came up (E.coli, Shigella, Cholera, etc.) were gram-negative. Is there is reason that that type effects the digestive system so often or is it coincidental?

Gastrointestinal infections can be caused by Gram positive and negative bacteria:
Gram-positive:

Staphylococcus aureus
Clostridium difficile, botulinum and perfringens
Listeria monocytogenes
Bacillus cereus

Gram-negative:

Salmonella enteritidis and typhi
Campylobacter jejuni
Shigella
Escherichia coli
Vibrio cholerae and parahaemolyticus
Helicobacter pylori
Yersinia enterocolitica

Any part of the GIT can be infected by G+ or G- bacteria:

Stomach: S. aureus (G+), H. pylori (G-)
Small intestine: Bacillus cereus (G+), Salmonella enteritidis (G-)
Colon: Clostridium difficile (G+), Shigella (G-)

Certain bacteria typically affect only certain parts of GIT: H. pylori and S. aureus affect mainly the stomach; C. difficile affects mainly the colon.
Anyway, infections of the gastrointestinal tract are much more commonly caused by Gram negative than positive bacteria (Stat Pearls, 2019).
From the pathogenicity viewpoint, the main difference between Gram-positive and negative bacteria is that G+ bacteria produce exotoxins (which are proteins that bacteria secrete into their environment), while G- bacteria produce endotoxins (which are lipopolysaccharides as parts of bacterial walls). The differences between endo- and exotoxins (microbiologyinfo.com):

Endotoxins are heat stable, so they are not destroyed by cooking, they don't need specific receptors, they don't trigger antibodies and there are no vaccines against them.
Exotoxins are heat unstable, they trigger antibody response and have specific receptors in the GIT.

More than 80% of skin infections is caused by Gram positive bacteria, such as Staphylococci and Streptococci (Clinical Infectious Diseases).
75-95% of uncomplicated urinary infections (Microbiology Spectrum) and most sexually transmitted infections (Clinical Laboratory Science) are caused by Gram-negative bacteria.
Respiratory infections are caused by both Gram-positive and negative bacteria (Lumenlearning).
So, the only pattern I see is that in dry/air-exposed areas (skin, respiratory tract), most infections are caused by Gram-positive bacteria, and in wet areas (gastrointestinal and genitourinary tract) by Gram-negative bacteria. This doesn't mean that there is any actual biological mechanism behind this pattern, though.


text:
How is vitamin B12 stored in the body although it is water-soluble?
Vitamin B12 is stored in the liver for a long time.
How is it stored?

Compounds are not necessarily lost from the body just because they are water-soluble. Cell membranes serve to sequester water-soluble molecules in the cytosol. It more depends on whether cells have transporters or binding proteins that lets them retain a given compound.

Yeah ! I researched about that . That's why I deleted the last comment. Thanks for your answer

Vitamin B12 (cobalamin) is a cofactor required by the enzymes methionine synthase (MTR) and methylmalonyl-CoA mutase (MUT). These are the only known enzymes that use B12 in humans, and are abundant in the liver. Since it is a cofactor, B12 is not consumed by any reactions, and hence there is no need to store large amounts of B12 beyond that bound to MTR and MUT. (In contrast to major nutrients like glucose and fats, which are stored in large amounts.)
Early biochemical studies showed that B12 isolated from cells was bound to an unknown large protein complex, called the intracellular cobalamin binding protein (ICB). It was later found that ICB actually consisted two separate proteins, and that these were identical to MTR and MUT.
So B12 is "stored" by simply being attached to the enzymes that require it. But, as @jzx also pointed out, perhaps "storage" is not an accurate description --- cobalamin is an integral part of these enzymes; it is not present in excess, and not kept in some storage compartment from where it can be mobilized (like glycogen, for example).

B12 is stored as mitochondrial 5-deoxyadenosylcobalamin, primarily in the liver (2 to 5 mg) but also about another 1/3rd in muscle. It's estimated that 0.1% of reserves are turned over per day, and the reference values for serum B12 are 180 to 914 ng/L.
While the literature tends to use the term "storage," this coenzyme form of B12 would still be taking an active role in metabolism. As the liver and muscles have the most mitochondria per cell, they are apparently considered the de-facto reserves.
Note that my source (1) indicates that it wasn't fully understood how this stored AdoCbl is released.
Source:

Nutrient Metabolism: Structures, Functions, and Genes. 2015.
Mayo Clinic: Vitamin B12 Assay, Serum

A good start, but how is the vitamin stored? Is there a major binding protein, for example? Also, I think the 5-deoxyadenosyl form is a radical that occurs in some reaction mechanisms, so I doubt that is a storage form. To my knowledge, adenosylcobalamin and methylcobalamin are the two forms that are active cofactors.

It does seem like "storage" could be a misleading term. Admittedly, it might be more correct to say that it's stored in several forms if you were to take a broad view of the process.

I think that's right. I posted a second answer just to detail the binding proteins a bit more.


text:
How long does the Ebola virus remain infectious on contaminated items or surfaces?
I'm sure there will be variation depending on what the contaminated item or surface is made of - linens, I could imagine, would remain dangerous for longer than a door-knob. But if the items are not decontaminated in some way, how long can the virus survive outside a host?

This really depends on the environment, one study (listed below as reference 1) found that the Ebola virus can survive under ideal conditions on flat surfaces in the dark for up to six days - see the figure from the same publication.

However, the virus is quite sensitive to UV radiation (see reference 2 for all the details) and most viral particles are likely to get inactivated within relatively short time. It might still be possible to get positive tests for Ebola from really sensitive PCR-based tests, but these are most likely not infectious anymore. The CDC lists common bleach (or any other routinely used disinfected) as a good way to get rid of Ebola viruses.
References:

Persistence in darkness of virulent alphaviruses, Ebola virus, and
Lassa virus deposited on solid surfaces
Sensitivity to ultraviolet radiation of Lassa, vaccinia, and Ebola
viruses dried on surfaces

From how many particles does it cause disease? (I forgot the exact term. :S)

Using % and log on the same graph... sigh ...

I found this safety sheet in the topic.

SECTION IV – STABILITY AND VIABILITY
DRUG SUSCEPTIBILITY: Unknown. S-adenosylhomocysteine hydrolase
  inhibitors have been found to have complete mortality protection in
  mice infected with a lethal dose of Ebola virus (30).
DRUG RESISTANCE: There are no known antiviral treatments available for
  human infections.
SUSCEPTIBILITY TO DISINFECTANTS: Ebola virus is susceptible to sodium
  hypochlorite, lipid solvents, phenolic disinfectants, peracetic acid,
  methyl alcohol, ether, sodium deoxycholate, 2% glutaraldehyde, 0.25%
  Triton X-100, β-propiolactone, 3% acetic acid (pH 2.5), formaldehyde
  and paraformaldehyde, and detergents such as SDS (20, 21, 31-34).
PHYSICAL INACTIVATION: Ebola are moderately thermolabile and can be
  inactivated by heating for 30 minutes to 60 minutes at 60ºC, boiling
  for 5 minutes, gamma irradiation (1.2 x106 rads to 1.27 x106 rads),
  and/or UV radiation (3, 6, 20, 32, 33).
SURVIVAL OUTSIDE HOST: The virus can survive in liquid or dried
  material for a number of days (23). Infectivity is found to be stable
  at room temperature or at 4°C for several days, and indefinitely
  stable at -70°C (6, 20). Infectivity can be preserved by
  lyophilisation.

2010 - Free Safety Data Sheet Index - Ebola virus

However there are no references on the site, so I checked the data provided. According to scientific articles it is trusty, however these articles are related to not the current West African strain, so it can be slightly different.

1982 - Inactivation of Lassa, Marburg, and Ebola viruses by gamma irradiation.

Clinical specimens from patients infected with Lassa, Ebola, or
  Marburg virus may present a serious biohazard to laboratory workers.
  We have examined the effects of heat, alteration of pH, and gamma
  radiation on these viruses in human blood and on the electrolytes,
  enzymes, and coagulation factors measured in laboratory tests that are
  important in the care of an infected patient. Heating serum at 60
  degrees C for 1 h reduced high titers of these viruses to
  noninfectious levels without altering the serum levels of glucose,
  blood urea nitrogen, and electrolytes. Dilution of blood in 3% acetic
  acid, diluent for a leukocyte count, inactivated all of these viruses.
  All of the methods tested for viral inactivation markedly altered
  certain serum proteins, making these methods unsuitable for samples
  that are to be tested for certain enzyme levels and coagulation
  factors.

1984 - Physicochemical inactivation of Lassa, Ebola, and Marburg viruses and effect on clinical laboratory analyses.

Ebola, Lassa, Venezuelan equine encephalitis, and Sindbis viruses were
  dried onto solid surfaces, incubated for various time periods under
  controlled conditions of temperature and relative humidity, and
  quantitatively eluted from surfaces, and viral titers in the recovered
  samples were determined. The viral inactivation kinetics that were
  obtained indicated that viral resistance to natural inactivation in
  the dark follows (in decreasing order of stability) alphavirus > Lassa
  virus > Ebola virus. The findings reported in this study on the
  natural decay in the dark should assist in understanding the
  biophysical properties of enveloped RNA viruses outside the host and
  in estimating the persistence of viruses in the environment during
  epidemics or after an accidental or intentional release.

2010 - Persistence in darkness of virulent alphaviruses, Ebola virus, and Lassa virus deposited on solid surfaces

Our study has shown that Lake Victoria marburgvirus (MARV) and Zaire
  ebolavirus (ZEBOV) can survive for long periods in different liquid
  media and can also be recovered from plastic and glass surfaces at low
  temperatures for over 3 weeks. The decay rates of ZEBOV and Reston
  ebolavirus (REBOV) plus MARV within a dynamic aerosol were calculated.
  ZEBOV and MARV had similar decay rates, whilst REBOV showed
  significantly better survival within an aerosol.

2010 - The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol

Any explanation about downvote?

What does  found this safety sheet in the topic mean? Link?

@not2qubit I wrote a quote and a link right below that.


text:
Do trees grow from the bottom or the top, or is that oversimplifying?
I was wondering how trees grow. I wonder if it was similar to hair growth which occurs from the follicle. but clearly branches grow from the trunk so there is definitely a difference with hair growth.
I looked here and couldn't find a verifiable source, there are contradicting answers.
Here it says trees grow from places in places called meristenes, and it denies trees grow from the bottom, but more like from the branch tips and root tips.
If I carve and inscription in a young tree, will it get up with time?

Wikipedia / meristem

It appears you are mostly interested in the vertical growth of trees. As @Joe Healy points out, this is done only by cells in the apical meristem. This region always remains at the top tip of the tree, that is where the upward growth occurs. The apical meristem, as it continues upward with growth, will leave portions of itself behind that may result in branches (axillary merristems). So yes, unless you carve at the very tip of the tree, your initials will remain at the same height you carved them.
A very simple experiment that I've done many times with students demonstrates this. Germinate some corn seeds until the shoot and the root are about 2 cm long. With a fine Sharpie, mark each with lines every 4 mm or so. Continue the germination. After a few more days you'll note that the line spacings nearest the kernal are the same as when you drew them. But on the very outboard end, near the tips of shoot and root, the spacing will appear stretched out.
Another type of meristem, the vascular cambium, is responsible for the increase in diameter of a tree. It is a sheath that lies between the bark and wood producing new wood to the inside and new bark to the outside.

Yes in general a tree's primary direction of growth will be from the tip of a new shoot, though not exclusively (for instance the additon of new tree rings occurs from the inside out.
Most growth occurs at the apical meristem of a new shoot as cells continually push outward.


text:
What about a bat's immune system protects them from Ebola?
Current evidence indicates that fruit bats are a reservoir host for Ebola. Has any research established what is different about their cell biology or immune system that reduces virulence for them?
Failing research on this particular system, do you have an example in another system of how virulence is reduced in the reservoir host?
I'm teaching a cell biology class, so actual examples of modified proteins or enzymes or inflammatory molecules in the reservoir is preferred.

New paper in eLife you might find interesting: Pigot et al. 2014. Mapping the zoonotic niche of Ebola virus disease in Africa. @Chris

@fileunderwater Interesting, thanks for the paper.

The main reason for this is that fruit bats are most likely (I don't think there has been a direct proof for Ebola so far) the reservoir host for this disease. The reservoir host is adapted to the disease and can harbour it for an indefinite time (with recurring infections) without showing signs of an infection or being affected by it. Although it is not getting sick, the reservoir host can pass the disease to other animals.
There is very little known about the immune system of bats, but they seem to be different, so they are not affected by diseases which cause havoc in humans. The following papers go into some details and they are interesting to read:

Bats: Important Reservoir Hosts of Emerging Viruses
Bats and their virome: an important source of emerging viruses
capable of infecting humans.

These papers give an interesting view of the bats immune system. The first article is a short explanation of the most important findings of the second. It looks into differences between species and analyse how the bats immune system may have evolved. Really interesting.

Of bats, flight and immunity to viruses
Comparative analysis of bat genomes provides insight into the
evolution of flight and immunity.
Antiviral Immune Responses of Bats: A Review


text:
What is an appropriate measure of determination in genetic studies?
Main Question
What is an appropriate measure of determination in genetic studies?
I used to think that $R^2$ was such a measure, but I'm no longer so sure. Specifically, it seems that $R^2$ undermeasures low determination and overmeasures high determination.
The reason for my doubt in $R^2$ comes from the following simulation.
Simple model
For simplicity, let us assume that a characteristic such as height (weight, Intelligence Quotient, Autism Quotient, etc.) of an individual is inherited from a mother and a father in the following fashion:
(fathersHeight * fathersInfluence + mothersHeight * (1 - fathersInfluence))/2,
where fathersInfluence is a constant between 0 and 1.
To give a specific example, if mother is 170 cm and father is 190 cm, and fathersInfluence is 0.5 then we know that their child will be exactly 180 cm.
Let us further assume that we can only measure the characteristic of any father and any son. We can not measure the characteristic of any mother.
Let us say that we'll try to predict son's height from father's height using good old linear regression, and report how much of son's height is determined from father's height. This can be done easily enough in python
_, _, r_value, _, _ = scipy.stats.linregress(fathers, sons)
Entire simulation can be wrapped up into the following python function:
def sonsHeight(sampleSize, fathersInfluence=0.5):
    # loc = mean
    # scale = standard deviation
    fathers = scipy.stats.norm.rvs(loc=170, scale=10, size=sampleSize)
    mothers = scipy.stats.norm.rvs(loc=170, scale=10, size=sampleSize)

    def weightedAvg(fathersHeight, mothersHeight):
        return (fathersHeight * fathersInfluence + mothersHeight * (1 - fathersInfluence))/2

    sons = [weightedAvg(father, mother) for father, mother in zip(fathers, mothers)]

    _, _, r_value, _, _ = scipy.stats.linregress(fathers, sons)
    return r_value ** 2

If we take fathersInfluence = 0.5 I would expect that any successful measure of determination would report that father's height determines son's height in 50%. $R^2$ passes this check, running the simulation with 1 million sons and fathers gives:
>>> size = 1000000
>>> print(sonsHeight(size, fathersInfluence=0.5))
>>> 0.500071151111

which seems reassuring. However, the values of $R^2$ for fathersInfluence any different than 0.5, seems to converge in probability to unexpected values. In fact running the experiment 101 times, for values of fathersInfluence from 0 to 1 in steps of 0.01 we get the following nice curve, which reassuringly passes close to $(0, 0)$ and $(1, 1)$, but surprisingly is not a straight line!

It becomes more disturbing though when particular values of $R^2$ are looked at, especially for fathersInfluence close to 0 or close to 1 (all $R^2$ come from taking a sample of 1 million).
In particular, for small values of fathersInfluence, say
$0.01$, $0.02$, $0.03$
the values of $R^2$ look close to
$0.01^2$, $0.02^2$, $0.03^2$.
Even for fathersInfluence of $0.1$ the value of $R^2$ is scarcely above $1\%$!
fathersInfluence, R^2
0.01, 7.3243188318051775e-05
0.02, 0.00042435668897930067
0.03, 0.00097257546851807486
..., ...
0.1, 0.012287962714812851
..., ...
0.97, 0.99904501126494283
0.98, 0.9995837493389228
0.99, 0.99989808360606525

Questions

Is there a measure of determination, which plotted against fathersInfluence would give me a nice straight line passing through $(0, 0)$, $(1/2, 1/2)$ and $(1, 1)$?
Would such measure be desirable?
What other measures of determination can be used, especially when the determination is low?

Remarks
I realize that the presented model of how genetics works is probably too simplistic and perhaps not useful as stated. However, I believe it resembles a good model for genetics in several aspects:

We have a thing that we can measure (e.g. gene expression level) and are observing as random noise important things we can't measure (environmental factors).
The independent variable (gene expression level) may influence the dependent variable (height, IQ, etc) only slightly.

All the code used to run this simulation can be accessed on github.

fathersHeight * fathersInfluence + mothersHeight * (1 -
  fathersInfluence))/2

is a terrible model for genetics. It says that the genetic contributions of the two parents are exactly anti-correleated. In fact they are essentially independent. I think what you are looking for is the notion of heritability.

The model is not anti-correlated, becasue fathersInfluence is a real number in the interval $[0, 1]$ and each parent's trait is positively correlated with the offspring's trait.

Your model says that the larger the fathers's influence, the smaller the mother's influence. Genetics only rarely works that way. You may be thinking some sort of  dominance model for a single locus, but height is a complex trait involving many genes. If dad contributes a height enhancing version of gene A, and mom contributes a height enhancing version of gene B, the contributions of the two genes will typically be additive but independent of each other. I urge you to read the Wiki article I linked too to see the basics of a real genetic model.

Thanks, I certainly will study heredity in some good detail. I perhaps haven't put across my point very clearly. mothersHeight is meant to be pretty much anything we can't measure (environmental factors, and other factors outside of our study). fathersHeight is the thing we can measure (expression level of a particular gene). fathersHeight is obviously going to have very small influence on the total outcome of the characteristic (most genes do in the end!), in the range of 1-2%. The point I'm raising is that R^2 will undermeasure this influence by a factor of ~ 100 for the 1% influence

It is very possible (and expected!), and I will definitely check it, that heredity doesn't suffer from this problem.


text:
Do viruses pickup new genetic sequences from the host cell?
Virus replication does not involve meiosis so the virus genome does not gain diversity from having two parents , so other than from mutation, do viruses obtain new genetic sequences from the host cell ?
Do virus genomes show evidence of containing base pair sequences which originated from host cell ?

look up the term "mutation" that is the source for new genetic sequences in sexual species as well.

Yes, it does seem that a virus can pick up transposable elements from the host — you may be interested in this related question: https://biology.stackexchange.com/questions/92829/do-any-known-viruses-contain-junk-or-parasitic-genomic-information

Yes.  See for example this article, which describes how some viruses can pick up bits of human DNA.  Here's a quote from the article:

...researchers have shown that a large group of viruses, including the influenza viruses and other serious pathogens, steal genetic signals from their hosts to expand their own genomes.

I really like that you gave an answer, but an appropriate quote from the article would make this answer soooo much better, earn you upvotes, and defeat the effects of a broken link.

OK, added a quote.  When I tested the link, it worked.  Is it broken from your perspective?

Nope. Perfect !

“Steal genetic signals” Obviously a case for the local constabulary.

It gets worse. The article in question reckons “they steal our genetic code”. Are you sure it isn’t a tweet from that flatulent person?


text:
How to measure bacterial content
I´m using water container placed on a radiator to humidify room air. Someone might argue that it is a perfect nest for bacteria. I have to put copper coins into the water to kill the bacteria.
I would like to do an experiment, have two similair containers filled with water one with copper coins, the other without them.
I would like to compare how many bacteria are living in those containers, how can I do that? (in home conditions)

There is evidence that copper pots have antibacterial effects when used for storing drinking water (Sudha, et al. 2012), so the copper coins will probably have a similar effect.
The easiest way to test this at home would probably be to buy a test kit from an online vendor - these are relatively inexpensive.
Some Googling produced this website [appslabs.com.au], which has some tests for common types of bacteria. There are undoubtedly others too, if these don't sound suitable

Anything I can get in Europe? Do you have any recommendation on type/brand?

@Hurda I'm afraid not - I've not used them myself, just found them by searching on the internet. Find one with some good reviews!

I think you might be better advised to try plating out samples of the water and counting bacterial colonies. There has been some good advice on doing basic microbiology at home elsewhere on this site.

I don't understand how this should help me to determine, which sample (container) conatined more bacteria before I started cultivation (and put any number to that)? Is it the speed at which the cultivation progress?

Thanks to leonardo for answering this before I got a chance to!

I have no idea, how your containers look like [and I doubt that's the best way to humidify air] and I don't think there is any chance to get rid of bacteria by putting some copper coins inside, but any-case:
The easiest way to measure concentration of bacteria utilized in laboratory practice is with the aid of a spectrophotometer. There are lots of protocols on-line, but basically you need a spectrophotometer able to measure absorption at 600 nm, special cuvettes and pipettes. One major drawback is that this way you get relative amounts of bacteria, and to get an idea, of how much cells in one unit of volume you actually have, you need calibration. [Calibration curves are unfortunately not transferable from photometer to photometer or from one bacterial culture to another one]. Calibration is generally performed by measuring absorption of media with different a priori known concentrations of bacteria. To get such control media, one needs a more laborious trick: measure individual cells from a known volume under a microscope (pour, say 1 mkl of the medium on a glass and "just" count all cells).
Moreover, you likely need a centrifuge, capable of rotating at 5000 g, because bacterial content in your water is not going to be high enough and you have to collect the cells and re-suspend them later in much smaller volume.

Few homes have a spectrophotometer, so this is not suitable approach "in home conditions" as was asked for.

Yes, perfect reason for a down-vote. I wrote: "in laboratory practice". E.g., I also don't have LB in my kitchen or a thermostate.


text:
Are efflux pumps mutations or are they originally present in N. gonorrhoea?
I'll start by saying that I am no biologist. I am a math major trying to create a mathematical model for gonorrhea strain competition. My assignment is to create a model similar to a model that was already was already created, see page 9 of Evolution of within-host Antibiotic Resistance in Gonorrhea.
I wanted to try to incorporate the efflux pump into a mathematical model. Before I do that, I would first like to see whether efflux is gained through mutations. If it is, my model will be pointless since mutations are already covered in the original model from the research paper.
Feel free to add better tags. I thought mine was appropriate.

Efflux pumps are common in bacteria, as well as eukaryotes. The mutations included in their model would not include efflux pumps. A mutation could potentially affect the efficiency of a pump in a strain but the mutations in their model are not creating the pumps.