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Could a trans-female person ever become pregnant?
I was told that a transgender person, which I will define as anyone assigned male or female at birth that identifies opposite to that assignment, could never become pregnant conceptually, due to the lack of hormonal pathways present in cis-male / trans-female person.
Are there modern medical methods that would allow for someone born male and is now trans-female to ever become pregnant or is it the case that medical science is not, nor ever will be capable of allowing for this?
Edit: I would say this is a different question than the suggested duplicate because someone who has AIS or CAIS would have a different anatomy than men assigned at birth, although not by much.

One thing I would point out in your question is that a female identifying as trans-male who has not undergone hormone replacement or reassignment can become pregnant, assuming there are no medical conditions that would prevent a pregnancy. It is only after they are trans-male that they would be incapable of becoming pregnant, unless of course their internal sexual organs were preserved. I think the bigger issue would be that as the person does not identify as female, they would probably not desire to become pregnant, either before or after reassignment.

Possible duplicate of Can androgen-insensitive genetic-males get pregnant?

@Christiaan The question here is phrased differently. It asks whether or not current medical technology could allow a trans-female to ever become pregnant. With Uterus transplantation, carefully controlled hormone therapies, in vitro fertilization, and cesarean delivery, the answer could be yes rather soon, though there may be some ethical hurdles to overcome.

Medical science has reached the point where it is able to consider performing uterine transplants in genetically female (cis-female) patients born without a uterus.
In the MedlinePlus report, First Uterus Transplant Planned in U.S. doctors at The Cleveland Clinic have plans to perform the first uterus transplant in the US sometime in 2016.
The article does however go on to state that the women will need to have been born with ovaries. The same matching process of blood and tissue typing that goes along with any organ transplant would still be in effect for this surgery.
It is also unlikely that the procedure would be open to women that lost their uterus due to cancer, as the recipients would be required to be on immunosuppression medication, and the risk of cancer recurrence would be too great.
As for your question about transplantation into Male-to-Female transgender patients, it is unlikely, at least with present technology that the person would be able to receive the transplant. There is a complex cascade of hormone signaling required for implantation of the embryo.
There could also be implications as to the formation of the placenta and how the person's body react to that. We have many examples of surrogacy, so we know that a woman can carry the embryo formed from the egg of another woman, but how the transgender person's somatic cells would react, given that they all have y-chromosomes is unknown.
According to a Yahoo! news article that interviewed Dr. Karine Chung, director of the fertility preservation program at the University of Southern California’s Keck School of Medicine and Dr. Christine McGinn, a New Hope, Pa., plastic surgeon who performs transgender surgeries on men and women, they foresee possibilities that this could happen in the future, however they do not cite any research that has been performed to date.
One of the issues would be the differing pelvic vasculature that a cis-male has to a cis-female, and what would need to be done to provide an adequate blood supply to sustain not only the uterus but the growing fetus as well.

...biological women have a leg up on biological males when it comes to accepting and nurturing a transplanted uterus. Women already have: vasculature needed to feed the uterus with blood, pelvic ligaments designed to support a uterus, a vagina and cervix, and natural hormones that prepare the uterus for implantation and support the pregnancy.
Men have none of those support systems — naturally — but none are impossible to create. “Male and female anatomy is not that different,” says Chung. “Probably at some point, somebody will figure out how to make that work.” (2)

The article does go on to point out that

Hormone therapy can shut off testosterone and introduce progesterone and estrogen needed to prepare the uterus for pregnancy.

Even though males do not have uterine veins and arteries needed to nurture the womb, it’s possible to attach a branch of a large vessel, like the internal iliac, to the uterus. “It’s doable, it just hasn’t been done,” Chung says.

Although it’s preferable for a vagina to support the uterus, it’s possible to attach a transplanted uterus to other ligaments in the pelvis.

So if I understand correctly we can not emulate the hormonal signals at all or well enough to allow for the formation of a placenta in a possible successfully transplanted uterus in a Male to Female transgender person? Is research being done in this regard or no?

I am not familiar with what is being done beyond the information contained in the article, and one or two others I have read with basically the same information. I would have to assume that to clear their Medical Ethics committee and gain approval for the procedure, the doctor's would have needed to limit the study to only women born without uteri. I do not know if they would have even gone so far as to consider the possibility of performing this procedure in the transexual population. As for what is being done elsewhere, this is the first I have heard of the procedure, so I cannot say.

The point of the ovaries is likely two-fold. First is likely hormonal, and the second is likely practical. If the woman has no ovaries, then she would not be able to give birth to a child that was genetically her's, so I would think that ethicists would weigh the risks versus the benefits as far too great to allow the procedure to proceed for the purpose of giving the person the ability to have the experience of being pregnant.

@RoSiv This article from Yahoo! news interviews doctors that feel that it may be possible within the next five to ten years, but here, they are guessing. https://www.yahoo.com/health/surgery-could-give-men-wombs-1302360099545142.html


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Protocol to dilute DNA step ladder?
I need to run gels that are of not the "most" importance. So I do not want to waste alot of money on step ladder. How do I dilute DNA step ladder? Is there a general procedure, for I have tried googling for one, but I get varying answers, such as a 1:4  dilution, and so on.
This is the information on the Step ladder, by Promega, posted as an image, since copy and pasting would mess up readability.

EDIT:
Even though I awarded the bounty because it gave me the same concept; what I had actually did was to assume I would use $60ul$ of ladder combined with $1$x dye.
Therefore since I started with $1ml$ of $6$x loading dye, $100ul$ of DNA step ladder, and available nuclease free $\ce{H2O}$, and I desired a 5:1 ratio of solution(dye and $\ce{H2O}$)  to ladder.
I would then use $12ul$ of stock to the $60ul$ total.
To make the dye $1$x, I would add $10ul$ of the $6$x dye to make the final concenetration of dye $1$x.
Then I would add up to $38ul$ with nuclease free $\ce{H2O}$.
So, sorry if this was worded redundantly, but It helps me to read, therefore in summary:
$$  +10ul  \text{ of 6x dye}$$
$$  +12ul \text{ of stock 100bp DNA step Ladder}$$
$$+ 38ul  \text{ Nuclease Free } \ce{H2O} $$
$$ \text{__________________________________}$$
$$\sum{60ul} \text{ of ladder & dye} (1 \text{x}) $$
of which total I can aliquot out to my hearts desire.
EDIT2:
The ladder turned out successful.

You'll probably have to titrate it down yourself. You might be able to estimate: The detection limit for ethidium bromide staining is about $1 ng$ per band. The insert says it's at "1 $\mu g/ \mu l$", but that's for all 40 bands and they're clearly not all at the same concentration. Depending on which bands you care about (1600 and below are dim), you might be able to get away with $(\frac{1}{25})^{th}$ their recommended concentration (1 $\mu g / 40$ bands = 25 $ng$) -- but I would titrate a small amount and see what works.

I am trying to visualize the mitochondrial cytochrome b gene of D. melanogaster if that is of any help in this endeavor. I dont think its a larger region according to Flybase.   http://flybase.org/reports/FBgn0013678.html        But to be honest I am a novice.

That gene is ~1 kb, and the ladder is maybe 1/4 as bright in that range compared to the HMW bands. Try diluting around 1:5 (add 4 ul of TE buffer or water per 1 ul of ladder).

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What evolutionary reason is there for hemolytic disease?
Nowawadays we have methods which allow us to overcome hemolytic disease of newborn or to prevent it to onset. The Rh or Kell conflict, but how is it possible that it is present? Why it haven't disappear due to natural selection?
A hemolytic disease occurs for example when mother have Rh- and the unborn child have Rh+ after his father. Then when the blood of the child gets to mother circulatory system she creates anti-Rh+ antybodies which will attack and eventually kill her next baby with Rh+. Thus we can assume that hemolytic disease is genetically dependent and cause lethal effect.
So i'm looking for any explanation. I know, that there can be none, i'm just asking.

You should have a look at the post Origin, or source, of rhesus negative in human blood (and eventually at Any evolutionary explanation for human blood groups?)

Disclaimer: I know nothing about hemolytic disease. I would suspect that not all babies of Rh+ and Rh- parents suffer from hemolytic disease. Do you have any reason to think that the variation babies have Rh+ and Rh-
parents to have the disease is due to genetic reason (or in other words, is the disease heritable among the subset of the population of interest)?

Yes, the first baby is "immune" to it, because due to that baby (to be more exacly due to the baby's blood during birth) mom start creating antibodies. If no blood gets to her sistem then there is no problem to the next Rh+ child. But if antibodies exists, then they can travel though placenta to the baby's body and attack him. The Rh is heritable so there is much bigger benefit in having Rh+ daughter. So yes, hemolytic disease as a disease isn't sctictly heritable, but the cause of it is but not as straight as typical genetic disease.

Plenty of undesirable conditions haven't faded away. It's not lethal enough is a reasonable answer, since you already know the genetics.

Hemolytic disease is not a genetic disease. It is a drawback of how the immune system works. In general, the overall benefits of having the immune system as it is right now are way higher than sporadic disadvantages, like the Hemolytic disease, that is why it is not counter selected. If instead of being a rare condition it would be a common one, then I would expect it to be indeed counter selected.

It is genetic. It's connected to the blood heriability.

Well, I would not call it genetic. The mother makes antibodies against the blood cells of the fetus. If the mother is Rh+ and the father is Rh- and the fetus Rh is from the father,  there is a chance of incurring in the disease. But being of any Rh type is not a genetic disease per se. I can't find any gene in the literature linked to the disease itself. But please link any study that suggest the opposite, I am not a master in this particular disease.

@GerardoFurtado It was a quick example but please, can you tell me what is wrong?

I see, I have swapped the Rh signs! The concept stays, it is not correct to call it a genetic disease, it's an immune disease.

just figured that out :)

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Question about cytoskeleton coordination
I am trying to study for a biology and I am having some confusion over the following topic. Can anyone help explain/ shed some light on the concepts of Rho family GTPases. Is it true that we have Rho activates forimins to relieve  auto inhibition of actin filaments while Rac promotes lamellopodia and Cdc42 works on the leading edge and fillipodia?
Secondly, how are the microtubules involved in cytoskeleton coordination? Do they simply affect Rho and Rac concentrations. How else is the concentrations of these spread throughout the cell as to maintain distinct concentration gradients?
Thank you all for any help!

The dynamics of Rho GTPase activities are highly complex.. Try to read this article.. it could help you understand or it could make your confusion worst :P


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Should we induce fever to assist healing?
I am currently reading "The Fundamentals of Anatomy Physiology" 10th edition, and have found it an incredibly interesting book. I have just been reading about the lymphatic system, and the various Leukocytes and their roles. When it mentioned fever as an immune response, I was familiar with the concept: Bacteria and viruses operate very nicely at our usual body temperature, but not so well at around 39 degrees Celsius.
What I wasn't aware of was "For each 1 degree Celsius rise in body temperature, metabolic rate increases by 10 percent. Cells can move faster, and enzymatic reactions take place quicker." (Quoted from page 828 of that book).
Now that seems like a massive benefit (though I believe you could only really push 1 or 2 degrees before you start getting into dangerous territory), but I notice that fever is not present in all illnesses. Inflammation seems to induce fever through the wounded area, which makes sense.
So now for my question: Could it be beneficial to artificially induce fever in a person who has an illness if they are not already experiencing fever? I believe a few things would need to be considered (more than likely a lot more than I can think to list):

Increased metabolic activity would surely need a higher energy intake would it not?
Are there cells that are actually going to suffer from the temperature increase?
I'm assuming this would actually be a rather poor technique to deal with cancer as from my currently limited knowledge, it is simply a cell that is producing abnormal proteins. If this is the case, the metabolic increase would likely apply to these abnormal cells, resulting in faster proliferation. Are there other such cells/infections that will benefit from temperature increase?

Finally, what are possible downsides of long term fever if energy intake is sufficient to maintain an increased metabolic rate at these higher temperatures?

Could it be beneficial to artificially induce fever in a person who has an illness if they are not already experiencing fever?

No, not really. Pretty much the only use of hyperthermia in medicine is in the treatment of cancer. If you google "use of hyperthermia in medical treatment", you'll likely only find two kinds of hits: those for cancer treatment and those for malignant hyperthermia (a side effect of some psychotropic drugs.) The hyperthermia used to kill resistant cancer cells is high enough to destroy proteins (~113°-114°) and very localized; your entire body raised to this temperature would result in death very quickly. Lower (i.e. physiological) levers of "hyperthermia" (or hyperpyrexia) would not kill the cells.
At the turn of the century, there were many who believed in the therapeutic use of hyperthermia in the form of hot baths, hot springs, and even injection of infectious agents to produce fever(!), but the practice has fallen into disuse, probably because there were no studies which supported it.
However, hyperthermia isn't good for you; it is something to treat seriously. When the cause isn't known, the efforts used to treat it can amount to many unnecessary tests and treatments (as seen in the accident victim in the fourth reference. When it's present in a moderate amount, it can still be dangerous:

When fever occurs, many physiological stresses take place. Some of these include increased oxygen consumption as a response to increased cell metabolism, increased heart rate, increased cardiac output, increased leukocyte count, and an increased level of C-reactive protein. Oxygen consumption increases by 13% for every 1°C increase in body temperature, provided no shivering occurs. If shivering is present, oxygen consumption may increase by 100% to 200%. Some cytokines released during fever states also induce physiological stress. These cytokines can trigger accelerated muscle catabolism by causing weight loss, loss of strength, and negative nitrogen balance. Physiological stress can be manifested by decreased mental acuity, delirium, and seizures, which are more frequent in children.

It is likely beneficial in the presence of infection:

Heat shock proteins are one of the more recently studied fever-responsive proteins. These proteins are produced during fever states and are critical for cellular survival during stress. Studies suggest that these proteins may have anti-inflammatory effects by decreasing the levels of proinflammatory cytokines. Fever also triggers other beneficial effects, including an increase in the phagocytic and bacteriocidal activity of neutrophils and enhanced cytotoxic effects of lymphocytes. Some bacteria become less virulent and grow slower at the higher temperatures associated with fever. Increased levels of C-reactive protein promote phagocytic adherence to invading organisms, modulate inflammations, and encourage tissue repair.

In the absence of infection, there is no benefit to systemic elevation of temperature. For the disadvantages of continued elevated metabolic rate, one need only look at hyperthyroidism to see the deleterious effects, the worst being cardiotoxicity, even in subclinical hyperthyroidism, as well as dementia, atrial fibrillation, ventricular hypertrophy, miscarriage, perinatal morbidity and mortality, decreased exercise tolerance, etc.
Years ago, one of the most common self-inflicted illnesses was hyperthyroidism - people taking thyroid hormone replacement unnecessarily - usually because of the weight loss that occurs with elevated metabolic states. Interestingly, efforts are underway to isolste and manufacture a thyroid-hormone like substance which will cause decreased weight without cardiotoxic effects.
Hyperthermia in Cancer Treatment
HYPERPYREXIA PRODUCED BY BATHS
ARTIFICIAL FEVER IN THE TREATMENT OF GONORRHEAL OPHTHALMIA
Thyrotoxicosis in a patient with multiple trauma
Metabolic Effects of Thyroid Hormone Derivatives

"At the turn of the century, there were many who believed in the therapeutic use of hyperthermia in the form of hot baths, hot springs, and even injection of infectious agents to produce fever(!), but the practice has fallen into disuse, probably because there were no studies which supported it."  Not so. Julius Wagner-Jauregg  won a Nobel Prize given for his studies on malaria pyrotherapy. This approach was discontinued because of the advent of antibiotics, not for lack of evidence!

Hyperthermia isn't used for malaria--rather, patients were deliberately infected with malaria to treat syphilis because malaria induces high fever. Whatever the intent of your post, the claim "no studies...supported it" is badly at odds with the fact that a Nobel Prize was given for precisely such studies and so this seemed a correction worth making if we care about the faculty accuracy of biology.SE. More generally, having read a hundred or so recent studies about the effects of endogenous or induced fever on infectious disease clearance, I think you are dismissing hyperthermia too quickly.

@Corvus - there is nothing, I assume, preventing you from posting your own well-referenced, better answer?

Once I get my head around the subject fully I'll be happy to do so. It's not an easy topic to synthesize because there are so many individual facts and study results out there, and so little by way of coherent explanation for the entirety of the phenomenon. The evidence seems overwhelming that fever hastens viral and bacterial clearance, but despite numerous conjectures there is no decisive explanation for the causative mechanism by which it does this.

This has really helped me get a direction as to what I need to look at, so thank you very much for this! I shall look at all of the references as time permits and see what they say. @Corvus If you have some stuff you would like to add in to an answer with some other references and ideas, that would be good. The more information I have that indicates relevant areas, the better! Seems like hyperthermia has a huge affect on parts of the body, as I expected. It seems like the answer is something like: Yes it is good in some cases with side effects, and no in others.

@Corvus... You seem to hold the Nobel Prize up to some biblical standard... How about António Egas Moniz developer of the Prefrontal Lobotomy and 1949 Nobel Prize winner in Medicine in Physiology for "for his discovery of the therapeutic value of leucotomy in certain psychoses"? Wagner-Jauregg's treatments, while effective and a keystone in the development of neuropharmacological treats, were at best ethically questionable. Also he got lucky in that the cause of the Dementia was bacterial in nature. His research was looking to use fever as a cure for all forms of "insanity."

He used anecdotal evidence as the basis for treatment without knowing the  root cause of the problem. His "cure" worked because it happened to be caused by infection of a pathogenic bacteria. From what I read it does not appear that he knew that he was using fever to treat a bacterial infection that caused symptoms of dementia in syphilis. That doesn't constitute good science. Then there is this gem: "Other patients were deemed schizophrenic because of excessive masturbation, where Wagner-Jauregg sterilized them, resulting in an "improved" condition." from Wikipedia article on Wagner-Jauregg.

@AMR. As I thought was clear in my comment, the whole point of my mentioning Wagner-Jauregg's Nobel prize was to say that were experiments on this, and that they were in fact well known ones. I was not vouching for Wagner-Jauregg's science one way or the other. With respect to anecdotal basic of treatment, this is medicine, not science. One could make the same critique of Edward Jenner.

@Corvus In your rebuttal of anongoodnurse, you say "the claim "no studies...supported it" is badly at odds with the fact that a Nobel Prize was given for precisely such studies and so this seemed a correction worth making if we care about the faculty accuracy of biology.SE." This basically is saying that as a Nobel Prize was awarded, then the research which lead to the award was also correct, or even good. Moniz work was downright barbaric, but he won a prize. And based on what we know now of the immune system, the idea that hyperthermia was the curative agent is greatly suspect,...

if not disproven. The fact that an immune response was triggered and the leukocytes were called into action is far more likely a scenario. When the bacteria that cause neurosyphilis get into the CNS, they are in an immune privileged space, where, most of the time, WBCs cannot access. However with an infection as powerful as malaria, the immune response and all of the cytokines release make even the BBB somewhat leaky to immune cells, that can then hunt down and fight the infection. As with your reference to Jenner, they were on to something, but there wasn't proof for the mechanisms of cure.

However we likely won't know for certain, as medical ethics today would likely prevent patients from being subjected to treatment with a highly pathogenic parasite.

Also, according to the wikipedia article on Malaria, "...the inventor of this technique, Julius Wagner-Jauregg, received the Nobel Prize in Physiology or Medicine for his discoveries. The technique was dangerous, killing about 15% of patients, so it is no longer in use."

The wikipedia reference is from a Science news article from November 8, 2013 by Gretchen Vogel. It is behind a pay wall, so some of the highlights: He initially tried with tuberculin and salmonella toxin, but there was no effect. To which he thought the fever was insufficient. Then he had a patient with Malaria, so he draws their blood and gives the disease to 9 patients. 6 improved. There was only about a 50% recovery rate, and 15% fatality rate. That implies 35% either did not recover sufficiently or got worse but did not die. And "No one is sure exactly how it worked..."

@AMR "And based on what we know now of the immune system, the idea that hyperthermia was the curative agent is greatly suspect," Elaborate?

@sterid read Janeway's Immunobiology, then see if my statement makes more sense. Fever is a side effect of the cellular immune response, not a factor in the defense itself.

Fever: facts... is a dead link...

@not2qubit - It was fine 5 years ago; but thank you. It would be nice if it were still available.

Actually, hyperthermia is a known treatment for a range of diseases, including cancer.
Induced hyperthermia can be whole-body as well as local/regional and is under investigation in multiple studies (for example).

Those studies you linked to are quite interesting. I will look into some more recent studies and see what they have found. And thank you for referring to it as hyperthermia, it is a much more appropriate term!

This would be a much better answer if there was more than a yes/no, and a couple of links.

@anongoodnurse I found the links fairly helpful, but they related primarily to cancer treatment (which still nicely addresses something that I had a misconception about in my question). Are there any other things you could recommend I look into to better understand the concept I described?

@Stevo - I'll look into this and post something more comprehensive and balanced tomorrow (if no one else does!)

@anongoodnurse why do you delete your 10 comments? you should take the responsibility for your words and behavior.

lol, why did you delete yours? I deleted mine because they are not relevant to most users. But if you insist: This is a poor answer, with an opinion and a couple of links. SE strives for better. Please read "how to answer" in the help section for guidance on how to answer questions.

In terms of bacteria and viruses within humans, the reason the bacteria and viruses function well at normal body temperature is because it's normal.  If fever were a perpetual state, the bacteria and viruses would evolve to be fit at that fever state.
There is also reason to believe that one way aging occurs is through metabolism (https://www.sciencedaily.com/releases/2011/04/110427091949.htm).  Thus, perpetual fever would likely reduce life span.

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Why minimum infective dose of a virus is not just 1 particle?
I've stumbled upon a term "minimum infective dose" (for example, of HIV), but don't exactly understand what is it? Why it is not always equal to 1 virus particle? I expect 1 lucky virus to be able to start infection just like 1 lucky spark can start a fire.
The following options comes to mind:

Multiple particles of the same virus need to act in cooperation to trigger their reproduction;
There is some 100% working, but limited use immunity that knocks down first N viruses;
Infection probability lower than some theshold % is not considered by statistics.

In general, how infection probability and severity correlates with the number of particles? Is it linear (double the number of viruses => double probability or infection) or something trickier?

You just answered your own question. "I expect 1 lucky virus to be able to start infection just like 1 lucky spark can start a fire." How often does a spark - a single spark - start a fire? How many times will the flint be struck to get enough sparks that one will land on the exact spot needed to start a fire? The rest of your answer depends on the virus and the host.

Then it should be said not "minimum infective dose", but a "minimum dose that cause infection with N% certainity" or "probability of infection from a single virus".

The meaning is implied in the term. Remember that scientific inference is based on repeated observations. Observations closer to the mean are more likely to be given more importance than rare outliers.

From Merriam Webster:

the smallest quantity of infective material that regularly produces infection

(emphasis mine)
The word "minimum" here is not meant as a strict minimum it is meant as a statistical bound, the absolute probability for which depends on the types of tests done and their inherent accuracy/inaccuracy.
Reasons that this "minimum" is greater than 1 could include:

Probability that a given particle actually finds a suitable host cell, enters the cell, and replicates; failures can occur at many stages along that chain
Rate of immune system reaction/response. At low exposure levels, the immune system may detect and clear the infection at a rate faster than it can spread, such that the infection stays asymptomatic. Some vaccines use weakened or low doses of pathogens specifically to evoke an immune response. The intent is that the weakened pathogen will not spread fast enough to overcome the immune response and will not produce a full disease.
Clearance of the infectious agent before it reaches symptomatic levels. This probably applies more to bacteria but I don't see why it couldn't also apply to viruses. I think the best example is exposure to bacteria that cause gastrointestinal infections like E.coli or Salmonella. Small numbers may grow and multiply in the gut, but they grow slowly if they aren't present in a high enough concentration and they may pass through the gut before causing any noticeable symptoms.

The minimum infective dose can also vary from individual to individual or due to environmental factors (for example, see this paper).

Some additional references:
Leggett, H. C., Cornwallis, C. K., & West, S. A. (2012). Mechanisms of pathogenesis, infective dose and virulence in human parasites. PLoS pathogens, 8(2), e1002512.
Ward, R. L., Akin, E. W., & D'Alessio, D. J. (1984). Minimum infective dose of animal viruses. Critical Reviews in Environmental Control, 14(4), 297-310.
Yezli, S., & Otter, J. A. (2011). Minimum infective dose of the major human respiratory and enteric viruses transmitted through food and the environment. Food and Environmental Virology, 3(1), 1-30.

So unless there is exact probability threshold for the word "regularly" it is not a strict definition. Is it like 0.2% or 2% or 20% or 99.7%?

@Vi. Exactly, it is not a strict definition. Individual works that present a minimum infective dose explain their methodology.


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How predictably will RNA polymerase not transcribe repetitive sequences?
I am working on an (expensive) synthetic construct, which happens to have many "repetitive" sequences within it that are integral to its function. Primarily, the two sequences that are worrying me are:

A long polyA (about 15 nucleotides).
A consecutive sequence of two nucleotides: GGGUUUGGUUGU, etc.

I've heard from many some of the transcription horrors they've been through because of similar sequences with similar nucleotides. However, some advise that transcribing it shouldn't be a problem.
How predictably can RNA polymerase transcribe these sorts of sequences in E.coli?

I don't think repetitive sequences are intrinsically problematic to an E coli. Bacteria also deal with things like polyadenylation. Basically, you have nothing to lose from trying -- E coli is one of the more robust expression platforms, and it's difficult to predict whether the sequence will fold into some tertiary structure (which can easily impede translation.)
So I think the predictability should be set at the baseline for E coli RNA polymerase error rate, which is about $10^{-5}$.

Yes, transcription of a polyA sequence will be unreliable: for a repetition of 15 times the same nucleotide, the rate of transcription errors will be huge.
For example in E. coli, this paper http://www.ncbi.nlm.nih.gov/pmc/articles/PMC331007/ gives some order of magnitude of transcription errors caused by repeats of nucleotides. According to their data, for a run of 11 A (so shorter than yours), their are more than one third of transcripts with a frame-shift (deletion or insertion of one nucleotide).
In addition you may have bigger problems than transcription errors: your construct will also be extremely prone to frame-shift mutations. For example according to the data on figure 3 of http://www.ncbi.nlm.nih.gov/pubmed/22991466 by extrapolating to a run of 15 A, you can expect an indel rate higher than 10^-2 per base pair per generations. Because you have 15 target nucleotides it means that more than 10% of the cells will have a frameshift mutation leading to your gene not being functional.
I do not have data for 'A consecutive sequence of two nucleotides'.

Welcome to Biology SE! Your answer is welcomed, but we prefer more detailed answers where things are explained, statements are supported with references. Simply posting links to articles may not necessarily the best practice (while it is a good way to support your claims). Please elaborate your answer by processing the papers you linked, extract useful and relevant information from them, use your on words, quote if necessary. Feel free to visit our help center on guidelines for posting good answers. In this form it is rather a comment than a full answer.

I am not sure why 'This does not provide an answer'? I edited the post to add more precisions, but my answer remains the same: a polyA sequence of 15 nucleotides is a problem if it is 'integral to [the] function' as the author says.

I've seen mRNA delivery papers that make their mRNA using a plasmid with up to 150 As on the 3' end of the gene so they don't have to add the tail through a separate enzymatic reaction. However, being on the 3' end would probably prevent frameshift problems. I don't know how they get the As into the plasmid, I tried to order a 100 A DNA oligo from IDT so I could try to add it to a plasmid, but they wouldn't synthesize anything longer than a 30 As in a row.

@AliceD 's comment was before you edited your answer which by the was looks much better!

Great answer. +1 thanks for editing. Writing up the answer and answering the question is something else here at Bio.SE :)


text:
Neuronal coordinates of C.elegans
Is there a list of neural coordinates for C.elegans? I need it to build a 3D model.
Update:
What is available at the moment is:

full connectome for example, at openconnectome;
neuron description with images of relative position at wormatlas;
2d position data at dynamic-connectome.

Update 2:
I've created very simple 3d model that consists of three layers (left, right and center) based on neuron labels. This shouldn't be considered as a real biological, but better than nothing. Code and data is on github.

Clarification:
The question is still there, I've provided very basic model and everyone are welcome to use it. But it still would be interesting to get experimental results. I'll keep the question open in case someone could share the data.

Any research done already? Please share or the question may be closed as 'homework' (I removed the "lazy" part in your post, but that is exactly trhe reason why this question may be put on hold :-)

nice piece of work!

Now that you have done some analysis yourself, can you clarify your exact question. You seem to have answered it yourself; if not then add some details.

I've revoked the -1 after these edits.

The Worm Atlas you cited is NOT just a "model." The neuronal cell coordinates were determined from an actual 3-D reconstruction of a worm based on serial thin section electron micrographs.  The serial sections were manually digitized to permit annotation and analysis using computer graphics. The annotation (over a period of years) established the synaptic connectivity, published by John White et al. in 1986 in the Proceedings of the Royal Society of London.


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Can you recharge without sleeping?
Sometimes it's difficult falling asleep for almost an entire night. You might feel like getting up and being productive instead, or 'pull an all-nighter'.
Or you can try to simply lay in bed to relax and rest, even though sleep does not kick in. In this situation, you may eventually fall asleep, only to be woken by your alarm just an hour or two later. Upon waking from such short sleep you can feel completely wrecked.
It leaves me wondering if you would feel more rested if you didn't sleep for just one hour. Maybe if you could relax throughout the night without really sleeping, you'd feel more rested by the time your alarm goes.
But is it physically possible to recharge as if you were sleeping without actually sleeping?

wikipedia says:       https://en.wikipedia.org/wiki/Sleep                                                                                If sleep were not essential, one would expect to find:
Animal species that do not sleep at all
Animals that do not need recovery sleep after staying awake longer than usual
Animals that suffer no serious consequences as a result of lack of sleep

Hi Marc - this has received a number of close votes because personal medical questions, or questions relating to your own personal health, are considered off topic. To make this "on topic" just remove the references to your own situation, therefore any answers/recommendations cannot be misconstrued as personal medical advice (which the vast majority of people here are not qualified to give). Thanks!

I suggested a very radical rewriting edit in order to remove all "personal health problem" wording and thus have the question qualify for reopening. You don't have to accept it, of course. But I think that with it, your question has a chance of getting open again and gathering more answers.

Was the edit I made not sufficient?

No, you cannot. Although we don't know how sleep works, we know that lack of sleep is very devastating to the body, and nothing (including laying in bed relaxed but awake) can replace it. If a rat experiences 100% lack of sleep (somebody keeps it awake all the time), this will kill it sooner than 100% lack of food would. There are no wake-until-you-die studies in humans, but even reduced sleep has very bad effects, both cognitive (it impairs you similarly as if you were drunk) and physiological (metabolic changes: you need more energy for the same actions, and food intake increases disproportionally).
If you have insomnia (and yours sounds severe), you need to get it treated. There are different options depending on whether an underlying cause is found, and whether behavioral therapies turn out to work for you. There are no alternatives which replace sleep.
The above is just a summary. For a dry but very reliable source on sleep, see Principles of neural science (ed. Kandel et al), Chapter 51 written by David McCormick and Gary Westbrook. For a very good popular science book on the subject, see Sleep thieves by Stanley Coren, I can recommend it for anybody with insomnia.

Hi, this is a well-written answer, but can you include a few references (e.g. that lack of sleeps would kill you sooner than lack of food). Thanks!

@Luke I did. Kandell (or rather the chapter author, K. is the editor) says that part about the "kill you sooner". I don't think I can find the exact page because I have the Kindle edition.

Ok. Didn't realise that reference was for all the points due to the vague wording - my apologies, it is an interesting answer.


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Why can I see a light flicker when it's in my peripheral vision?
When I'm looking at an old CRT monitor or a worn fluorescent lamp, but not directly in the center of my gaze, the light from it seems to flicker. When I focus my gaze onto the monitor or lamp, the flickering stops.
Why can I see a light flicker only when it's in my peripheral vision?

Your retina contains both rods and cones. Cones are color sensitive, slow, and concentrated near the center of your field of vision. Rods are "light" sensitive, fast, and concentrated near the periphery. You want to be able to respond quickly to a threat "in the corner of your eye" without needing to see the color of the threat.
This is nicely explained by this diagram (source: http://hyperphysics.phy-astr.gsu.edu/hbase/vision/imgvis/retina.gif)

So when you see a CRT in the corner of your eye, your rods respond quickly enough that you can tell the light of the CRT is flickering. As you turn your gaze towards it, you get the higher resolution, color rendition of the cones - and lose the temporal resolution.

This explanation doesn't work in daylight, when rods are saturated. See also: Why is peripheral vision not bleached by daylight?


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Why are there ghost images of objects just out of focus
I have observed an interesting phenomena with my vision lately. I just think I have never reflected over this before but it might always have been this way.
I am nearsighted and have no problem with double vision as long as an object is in focus, either with or without glasses.
However when I take my glasses off and look at, e.g. my phone screen, and push it slowly just out of focus, there is a phase where multiple distorted weak ghost images appear before everything just becomes a more Gaussian like blur. It is especially clear with bright lines on a dark surface.
I do not believe that there is anything else wrong with my eyes, since as soon as an object is in a range where I can focus on it, all ghosting disappears.
I am interested in knowing if anyone else observes this.
But more interesting is what are the possible optical properties of the eye that contributes to this, or is it a property of how our brain processes the input from the eyes.

Could you generalize this question? Personal questions are discouraged here as this site is meant to answer questions of value to the community. If you can show this phenomenon is not only applicable to you, it is of interest here. Note I am happy to look into this :) In addition, personal medical questions are discouraged as we strongly urge folks to seek professional help. Until edited, therefore, I vote toclose this question. A +1 for the exciting topic though. If you reply to this post, ping me by using @AliceD, please.

I think it is a general question about the phenomenon. I just had to describe what I have observed. I am not looking for a diagnosis, I want to know the reason for what I have observed

@AliceD I agree with the OP that this is not a personal medical question but rather one asking about how the eye itself works.

@terdon agreed, but its too specific slash anecdotal to my taste

@AliceD All interesting questions and later scientific progress starts with one persons observation. This is not the same as Anecdotal evidence, since I do not claim that caise A leads to effect B. I an just asking for the reason why an observation is as it is.

@AxelOmega - yes of course, the question is whether that sort of question fits this site . I started a discussion on meta actually


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His Tag location in gene circuit
I am part of an undergraduate research group and we are trying to produce a protease in an E.coli gene circuit. We are not sure where to place the His tag in our circuit. The sequence is
...OmpA(gene)->linker->his tag->protease->Terminator->res site
Should the His tag be in this position, before the linker, or after the protease? OmpA is a outer membrane protein that will allow a protein to be taken to, and linked to, the outer membrane of the E.coli. Our fear is that the protease will not fold correctly and will be nonfunctional.

When you say gene, have you made sure that the stop codon is removed?

Usually the his-tag should be in the terminal. Why don't you express the protease as a separate cistron?

There are advantages and disadvantages to put His-tag both N and C termini. When you put a tag at a C terminus, you can purify the full length easily. If you are lucky, you could get full length products even if you put a tag at the N terminus. An additional sequence at a C-terminus may disturb functions of some proteins, but in most of cases, it would not be predictable.

We have removed the stop codon of the gene. We wanted to have the His tag attached to the protease in some way to use as proof of concept that they protease is being expressed on the outer membrane of the E.coli.

Then what, I think, you should do is put his-tag after the protease. Is the C-terminal of Omp-A on the outside?

OmpA is a outer membrane protein so it will bring the protease to the outside of the cell. I'm not sure I fully understand your question. There are other parts of the sequence before the OmpA. OmpA will be on the outside of the cell.

@KellyEckartt got it. I just wanted to know if the protease would be outside the cell (Can you add this to your question?). C-terminal tag seems safer, in this case, to me. If your objective is just detection then FLAG-tag may be a better idea.

Fusing your protease to the C-terminus of the OmpA will not diplay it on the outside of the bacteria because the C-terminus is facing the periplasm (the space between the outer and the inner E coli membrane)


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Do lunar rhythms have really impact on plant growth?
It is commonly known that lunar rhythms have influence on plant growth, and there are even lunar calendars to know when planting, pruning, transplanting, harvesting, etc.
I know that the lunar cycles affect the tidal patterns, and this consequently can affect the life of sea organisms like reef corals, fishes, etc., but I am very skeptical that this can affect the growth dynamics or plant physiology.
 I would like to know how it works from a scientific perspective, E.g. the temperature and precipitation are the main limiting factors on plant growth, but I'm curious if the moon light or its magnetic field can also be a limiting factor on plant growth.
Then my question is simple, the lunar rhythms really influence the growth of plants, if so, how?

Great question! I think there is a similar question on Skeptics.SE but I assume you want a more scientific perspective, correct?

@TanMath exactly! I would like to know it from a scientific perspective. I have added more details to my question.

Let me point you towards this 3-part blog post on howplantswork.com. There are quite some references in there. If you ask me personally: I think there is no scientific basis for the widely believed lunar influence on plant growth. Just superstition handed down.

It may be worth linking to the similar question on Skeptics.SE — note that the most voted answer there somehow contradicts the only answer here.

Great question! The way I will do this is by explaining a bit about what moon planting is, then I will go through the articles I have found one at a time, to provide the different persepctives on moon planting, as it is called.
What is moon planting?
Moon planting is a methodology of planting, in which the lunar cycles are used as guides to know when to plant.
How might it work?
The first article is a great article about a gardener who tried to do moon planting, but it did not work for her, until she realized she did it wrong. Then, she found out the logic behind why lunae planting works. It really doesn't have to do with lunar cycles. Here is her explanation:

Let’s look at a possible scenario. Gardener I is a moon planter; Gardener II isn’t. Both gardeners wait till spring to plant their beans. (No sensible cool climate gardener will plant beans in winter. It’s too cold for them to germinate, and many seeds will rot or be taken by ants.) But come the first warm spell Gardener II succumbs to one of the great spring urges and plants the beans at the first hint that spring has arrived. Gardener I, on the other hand, waits till the next good moon planting time before planting the seeds. Early warm spells are usually followed by another cold one… and again seed planted too early may rot. Even if it doesn’t, plants that suffer any set-back when they are young usually don’t do as well as plants that have flourished right from the start. (The set-back can be from cold, boggy soil, snail or scale attack — the effect is the same). So counterintuitively, beans that are planted later in spring will probably do better than beans planted too early.

The opposite works too when planting in autumn. By the lunar planting schedule, it is better to grow earlier, and since the soil is warmer, the plants will grow better.
In the second article, the author reviews the research done on the effect of lunar cycles on reproduction, germination, and more. However, only the work of a researcher, L. Kolisko, shows evidence for the benefits of lunar planting. Therefore, the conclusion was lunar planting are not significant to affect crop yield.
However, in another article, it shows that there are many cycles in plants that are affected by the lunar cycles and that for some organisms, the lunar cycles do affect reproduction, germination, and production of different metabolites. Therefore, lunar planting might have an effect in that way as well.
Conclusion
The conclusion is that lunar planting may actually work, but many scientists are debating about it. So in reality, we aren't 100% percent sure about it, because there is evidence supporting it, and evidence contradicting it.
References

http://danfingerman.com/skeptic/Moon_planting.pdf
http://www.howplantswork.com/wp-content/uploads/2009/07/beeson_1946.pdf
http://www.howplantswork.com/wp-content/uploads/2009/07/schad.pdf

good answer, however the first example is based on temperate ecosystems where the temperature is the first limiting factor, but what about planting in the tropics where the temperatures are almost the same during all year?. I was doing by myself some experiments in the Andean region with good and bad results. I did it because there is a strong ancestral tradition to planting with the moon rhythms, and all farmers do it specially with short-cycle crops (Eg. corn, potatoes, etc.) and also in lowlands with the bananas. but it is curious that has not been done much research in this field.

@DarwinPC good point, by the logic pointed out in the firsf article, then there would be no signficiant effect. However, there are theories about whether or not moonlight could affect plant growth. Do you want articles on that? Also, if you like my answer and it answers your question very well, if you want, you can accept my answer by pressing the checkmark button near my answer.

@DarwinPC Much research has been done, but many are biased. Some of the research papers aren't even true science, and more like pseudoscience with astrology.

The point with the germination timepoint is about timing, not about the influence of the moon.

@TanMath I like your answer but I will wait for other answers, I don't want exactly an articles list, rather more convincing answers based on true science.

Based on your Nature citation (the other one being popular science, the third a rather broad work mostly on animals) I dare say the consensus is there is no effect. if you are specifically interested in moon-planting, the kolisko 1939 citation in the nature paper seems the strongest lead to the contrary.


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Does 405 nm light set off phosphorescence in the eye?
While playing with a blue/violet laser (5 mW, 405 nm) tonight, I noticed that on dark, non-fluorescing surfaces, the beam reflection was trailed by what looked like a dimmer reflection of the beam. The effect was most easily observed when I moved the laser in a circular motion. The apparent 2nd reflection was not produced by a side lobe of the laser diode, as it always trailed the main reflection, regardless of clockwise or counterclockwise rotation. Also when I stop moving the beam, the second 'reflection' quickly merged with the main beam reflection.
I doubt it is caused by phosphorescence of the material (cloth) I was lasering, as it also showed up when I pointed the laser at the floor, other sorts of cloth and painted walls.
So, do rods, cones, visual purple or other eye components phosphoresce when hit with deep blue light?

Instead of phosphorescence, a more parsimonious explanation is the perception of afterimages. Afterimages regularly appear after viewing a bright stimulus. They occur in the same location in the visual field as the original stimulus, but lack clarity. Afterimages depend on the intensity and contrast of the original stimulus (i.e., they are more pronounced with bright stimuli in a dark environment), the time of fixation (i.e., longer fixation generate more persistent afterimages), and retinal adaptation (i.e., dark environments enhance afterimages).
After images are almost always the complementary color (negative afterimage) to the original stimulus, but can very briefly be the same color (positive afterimage) when viewing an exceptionally bright stimulus. A stimulus consistently produces the same afterimage, which varies in size based on the distance between the person and the background. After images are often revived by blinking.
Afterimages are thought to derive mainly from photobleaching of the retina, although cerebral processes may contribute too.
Phosphorescence in the retina has to be induced by injecting phosphorescent markers (Wanek et al., 2013). As far as I know, the retina is not autophosphorescent.
References
- Gersztenkorn & Lee, Survey Ophthalmol, (2015): 1-35
- Wanek et al., Curr Eye Res (2012); 37(2): 132–137

The main reflection of the laser off a dark surface doesn't appear all that bright. Your ref doesn't say whether after image intensity is wavelength dependent, but red and green lasers at the same rate of laser movement, both produce continuous light trails; persistence of vision. There's some funny kinetics going on with blue to generate a distinct trailing spot.

Blue cone pigment is coded by a gene less closely related to red and green pigments. Could be different adaptation kinetics.

So not phosphorescence, which is what I asked. Blue cone is far less sensitive than red or green: http://www.physicsclassroom.com/class/light/Lesson-2/Visible-Light-and-the-Eye-s-Response (It'd be nice to see units on that Y axis). But that doesn't explain why I see a trailing dot rather than a trailing streak as with other colors. Watching that dot merge with the main beam reflection after I stop moving the beam is truly an odd sight. Guess I'll go with funny kinetics for now.

@WayfaringStranger - generally the laser beam is only visible when there are scattering particles. Only the point of impact is seen on the ground, a beamer screen etc. But no, pretty definitely not phosphorescence. Thanks for accepting!

AliceD: Yes, this is all about the behavior of spots at the point of beam impact, and slightly trailing it depending how fast I move the beam, not smoke or dust in the air.

Did you try recording this on camera and stop the video at one point?
if the trailing dot is visible there, it must be some light, emitted by the material. if not, its an effect, caused by your eye.


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Why am I losing much more vector than insert DNA during RE cloning?
I've been cloning some inserts into a lentiviral vector (pBOB backbone) by RE digestion and blunting ends with T4 DNA polymerase.
After these steps, I usually load the digested product onto 0.7% agarose gel to isolate the expected size fragments.
Unexpectedly, during agarose gel separation the bands from the lentiviral vector are much less intense compared to the insert ones.
Having extracted the DNA from such a band, its amount is insufficient to pursue the ligation process (I'm getting around 0.5 ng/uL of vector!).
I have already repeated the digestion three times and always get the same profile. I've also been checking the DNA amount after each cloning step (e.g. RE digestion, fill-in) and I notice that the lentiviral vector DNA amount is always half the insert DNA, which is a sufficient amount to be ligated.
Having used the same reagents for either vector and insert DNA, I would actually exclude a technical issue, as I'm under the impression that there's something wrong with the lentiviral DNA. Of note, it is a purchased plasmid from Addgene which I have already checked by RE digestion.
Do you have any idea of what's going on? Also, do you have any suggestions about how to fix the problem?
Thank you in advance for your kind help!

Welcome to the site. Can you please provide more details on your procedure - how (method) are you checking the DNA amount (concentration?). What site are you digesting at and how are you sure that the vector:insert molar ratios are correct? Gel extraction is notoriously low-return (generally <10% of input), so how much DNA are you loading onto the gel?

Normally I only gel-run a small fraction of the digested vector purely to check sizing and then either purify from the rest, or omit a subsequent electrophoresis altogether once satisfied with initial testing of conditions. This to purify DNA from most of the reaction mixture using a commercially available column kit, after dephosphorylating blunt ends with say SAP. Agarose extractions just yield less recovery. Lentiviral vectors do tend to recombine specially if the initial bacterial strain used in transformation was not the recommended in the optimised Addgene provided protocol.

I have seen so many students getting stuck at cloning.
Alternative Strategies:

Linearize your vector with PCR (use polymerase with corrective activity like Pfu) using primers that face away from the insert site. This yields large amounts of blunt ended dsDNA. Extract from gel. Then get the insert in by blunt-end ligation.
Change the restriction enzyme using a mutagenesis kit to introduce another restriction site.
Change the restriction site (or homologous sequence for different cloning technique) by extending the insert and/or vector with PCR using primers with overhangs.
Switch to another cloning technology (TOPO cloning, LIC, SLIC, Gibson, Gateway).

Other suggestions:

NEB says: "CAUTION: Elevated temperatures, excessive amounts of enzyme, failure to supplement with dNTPs or long reaction times will result in recessed ends due to the 3´→ 5´ exonuclease activity of the enzyme."
If you have checked the vector with RE digestion it should be fine..? Did that check yield the same unexpected low yield pattern?
Sometimes it helps asking someone else to do the procedure for you. That way you can exclude an error on your end.
Sometimes the restriction enzyme/T4-pol is old. Buy new one.
NEB has a troubleshooting guide for cloning.

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


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Is it safe to publish a person's genome?
I recently went through the process of having my genome analyzed by 23andme, and received my raw data.
Its very interesting to me, and I want to share it with the world.
Is it safe to publish the raw genome to a public site, or are there reasons I should keep this information private?
What could someone do with the raw genome of another person? Outside of privacy concerns, is there any potential for malicious concerns from someone with this information?

This is how the clone wars begin.

Welcome to Biology.SE. Here, we only deal with Biology question, not with questions of personal safety, information security, future political decision or justice. Your question touches all these fields and it is hard to imagine what SE site would be welcoming your question. Maybe informationSecurity.SE.

I would assume that this question is off-topic on Biology.SE, but I am unsure. 2. It's not a 'raw genome'. It's information based on an extremely limited number of ascertained variable sites, referred to as SNP genotypes. 3. The fact that you ask this very question should make you not give away the data. If I were you, I would - if I wanted to tell people about it - give away the major findings (e.g. ancestry estimates) without giving away actual variant data.

@Kritner I am not willing to go into a star wars argument, but I don't think the clone wars have anything to do with making genetic data public or not :)

I believe this topic is on-topic for Biology.SE due to the specific knowledge required to understand the implications of my question. Other sites not filled with experts in the topic may mis-inform me

@AndrewDiamond The fact that it takes some knowledge in science and economy to discuss whether a country should build a new nuclear reactor does not make the discussion of the decision purely scientific or economic. It remains within the field of politics. You can ask us specific question that are purely scientific that will eventually help you take your decision though.

There is some debate, about which I'm not very familiar, over whether or not health insurance companies should have access to such information. If the data reveals a genetic disease, it could be the basis to reject coverage.

It is as safe as to publish your fingerprints. Right now, there is little that anyone can do with your genetic information but in the future, this will change.
One of the feared consequences it concerns what companies may do with that information. Can it be used against you? In some cases, it may.
For example, if you have a predisposition for a genetic disease, then an insurance company may find a way to refuse to insure you. As far I know, right now this is illegal, but you never know.


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BLAST(Basic Local Alignment Search Tool) is heuristic?
How can we say that BLAST is based on a heuristic algorithm, as after finding one common word in the query sequence and a database sequence it performs pairwise alignment by dynamic programming - which is an exhaustive algorithm? Also, BLAST provides quantitative analysis by giving bit scores and E-values. As it gives quantitative results, why do we say it is based on a "heuristic algorithm", such as 'word algorithm'?

I didn't quite get what you meant by "word algorithm" - if it's important to your question, you may want to expand on that point.

You might be confused about what "heuristic" means. "Heuristic" doesn't mean random or arbitrary, instead, an algorithm is termed "heuristic" if it employs a shortcut which means that it does not necessarily yield the theoretically best result.
For BLAST, this shortcut is the assumption of first matching the fixed-length words prior to extending the match. Hypothetically, there could be a query sequence and a database where the best scoring match for the query sequence doesn't contain any k-length sequences in common with the database sequence. In this case, BLAST would be unable to find that match. - So the heuristic portion of the algorithm isn't in the dynamic programming portion, it's in that first step of finding pairs which are to be aligned.
The failure of BLAST to find a match is likely to be rare, though, especially with short word lengths. If you find a decent match, it's highly likely that there is a 3-mer (5-mer, etc.) of identical sequence in the pair. But because it's not a guarantee, the use of k-mer word in the process means that BLAST is a heuristic algorithm.
The ability for BLAST to provide quality and statistical metrics is not limited by its heuristic nature. To build an e-value, you don't need to know that BLAST is able to find the absolute best match. Instead, you just need to be able to build a model of the sort of matches BLAST would find by spurious random chance, when applied to a similar database with no "true" matches. Similarly for bit-score. You don't need to know what the absolute best match would be, you just need to know how BLAST would behave on a hypothetical true-match-free database of similar properties.


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Does opening the lid of the spectrophotometer affect my results?
If I'm performing an experiment using a spectrophotometer and I mistakenly forgot to close the lid on the spectrophotometer, would that affect my results?

ambient light from the room can leak into detector and create artifact in reading. best way to test it is to record absorption without sample and open lid.

It depends on the construction of the spectrophotometer, the wavelength of light you're detecting, and the sensitivity/accuracy that you're demanding of the result.
In the past I have used spectrophotometers which were completely missing their sample lid, with no appreciable detriment to the result. Several things were in my favor, though. The light path from the sample to the detector was suitably collumated, such that any light that wasn't coming from the sample was blocked. I was attempting to detect far UV wavelengths (e.g 260 nm), for which there is little to no ambient source - attempting to detect a wavelength at the peak of a fluorescent light wouldn't have been as successful. I also didn't need highly accurate results, and I was able to dilute my sample such that it fell within a region (~50% absorbance) that is least sensitive to small changes in the amount of light being received.
In your case? If you can retake your measurement "properly", then I'd recommend doing so. If not, you can run some tests (like user aaaaaaa suggests) with some other similar sample, seeing if the absorption readings for that wavelength are affected by having the lid open.


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Question regarding research project on indigenous ants during Eastern European winter
I am by no means biologist (I'm a programmer), but I want to make an experiment that involve the participation of ants. So please excuse my ignorance on the subject and my potentially uninformed questions.
I need to find some ants, but it's fall/winter here in Eastern Europe, so it seems that I won't be able to find in the wild. So my questions are:

If I find a species that is local (meaning that it's used to live through winter - maybe entering some kind of lethargy?) is it just putting them in high temperature enough to get them out of this mode?
Probably depends on the species, but if I take just few individual workers without a queen, and provide them with food, is it possible for them to live without a queen? Clearly they won't reproduce so their "colony" will disappear, but are the individuals able to live for a while without a queen?

If that is enough for you, you can actually buy complete ant farms.

Do you have any specific reason for using a wild species? If not, you would have better using a lab lineage (or any ant farm). Breeding a wild species by yourself might be very tricky.
Taking care of an ant colony might not be as easy as you may expect. Your best chance is to target a species of interest based on past studies and visit a lab that is breeding this specific species.


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How is tolerance to an allergen developed?
My question is mainly about how allergy shots work.
I did some basic research before posting here, however I could not find an explanation of what occurs at a cellular level.
Is it the persistance of the antigen which somehow induce immune tolerance?

The allergy shot in itself is a form of therapy called allergen immunotherapy (AIT). In it's essence, we're trying to get someone to develop immunologic tolerance to a given allergen such as pollen, okay! So how does it happen at the cellular level? (Assuming the treatment protocol is known)
Understanding The Mechanism Of Allergen Immunotherapy, as an article is kind of a broad overview. Thus there are phases to AIT that include early, intermediate and late phases. The process begins with a downregulation of mast cell and basophil activity, followed by induction of allergen specific Treg cells, a decrease in Th2 cells, and then a decrease in IgE production with an increase in IgG4/IgA.
Mechanistically, it doesn't look like it's well known how basophils and mast cells get regulated by AIT, but the theory is that the mechanism may resemble H2R (a histamine receptor) receptor activity during venom immunotherapy: H2R becomes highly upregulated after therapy start, and inhibits Fcε-R1 activation of mast cells and basophils, even in the presence of IgE (2, paywall on this one).
They provide an impressive table in Akdis & Akdis 2014 as to the role of immune cells in AIT:

So in the process of encountering the allergen, the immune system produces Treg cells as a result of dendritic cell antigen presentation. An inducible type of Treg called Tr1 is capable of abrogating the response of Th2 and Th1 cells through the secretion of TGF-ß and IL-10. They have a good table for this, too:

There's an effect in there due to TGF-ß exerting its effect on B cells that ends up inhibiting class switching to most other immunoglobulins except mucosal IgA. In conjunction with IL-4, IL-10 is capable of promoting the class switch of preceding B cells to IgG4. So the classes of Ig will largely become IgG4 and IgA in response to the allergen of interest. The B cells will also begin to produce their own IL-10, and in a way become a regulatory type of B cell, or Breg, that propagates the tolerogenic response.
And so the big conclusion: (1) the mast cells/basophils aren't as prone to causing anaphylaxis, (2) the effector cells specific for the allergen have actually shifted to populations of tolerogenic DCs, Tregs and Bregs, and (3) antibody production has shifted to IgG4/IgA from IgE. The net result is due to the repeated exposure to the allergen at some optimal concentration, but the key is they performed the treatment slow enough that the immune system had time to build up tolerance without going crazy. It's also likely that we don't know how long the system stays tolerant for after successful treatment.
It's much more complicated and if you can get past the paywall on source 2 there's really good, detailed info. I didn't want to go into a novel here, but let me know if you need clarification anywhere.


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"Signal Advance": Unsure of meaning or contextual use
I am reading through Recombinant DNA; Genes and Genomes - A Short Course - Third Edition by James D. Watson, et. al. and I came across this paragraph in the discussion about discrete factors of inheritance in Mendelian genetics:

The character shown by a plant depends on the pair of factors it receives from its parents. If both factors it receives are the same, that is, two dominant (yellow seed) or two recessive (green seed), then the plant exhibits those traits - yellow seeds for the former and green seeds for the latter. If one factor is dominant and the other recessive, then the dominant character is expressed; in this case, a plant with a factor for yellow seed and one for green seed will show the dominant trait, yellow seed. But the factor for green seed persists, even if the plant is yellow, and can reappear unchanged in later generations. This was a signal advance. In the 19th century it was believed that the traits of parents were blended in their offspring and, once mixed, the contributing traits could not be recovered. At the time, this was a severe problem for Charles Darwin's theory of evolution through natural selection. His critics pointed to that any favorable variation arising in an individual would have no long-term effect, because it would immediately be lost by blending.

Note: Added emphasis is mine.
I have done both Google and Google Scholar searches for

Signal Advance
Signal Advance Biology
Signal Advance Genetics
Signal Advance Science

and I have not had much success finding a definition for the use in this context.
One article, Plant biology: Signal advance for abscisic acid was one of the only relevant references I could find that used the words in combination, however they were only used in the title.
I am not sure of the context that it is being used in Recombinant DNA or in the plant biology article.
Are they saying that the signal advance marked a change in thinking on the subject, the way we would use the terms paradigm shift or quantum leap?
Or are they instead using the term in the sense of the recessive gene being maintained in the genome and was able to be expressed in future generations?
I have not come across the use of the term signal advance before, and it is difficult to work out from the context as the first half of the paragraph speaks about the genetics and then the second paragraph discusses how it provided evidence to change the hypothesis of the day.
There is a similar problem with the plant biology news and views as it talks about six new papers on a topic that had been elusive, but as it happens to be about a signaling pathway; I am left wondering the context here as well.
If anyone has come across this before and can help to clarify it for me, I would appreciate it. Thank you.

I almost wonder if this isn't a typo for 'singular'. I have no idea but I am curious.

@Resonating I do not think that they meant singular. Your question made me think about the grammatical structure of the Watson sentence, and it seems to be Signal as adjective and Advance as noun. When I looked at the definition of Signal as an adjective, there is this unusual; notable; outstanding: I think that both authors may be using it in this regard, but I still want to see if there might me a biological perspective to it.

@AMR you are essentially correct in your interpretation. "Signal" is a Britishism meaning key or important or groundbreaking. I think it's a bit old-fashioned, as I haven't really seen it much in contemporary literature, but I may be wrong on that part (I'm 'Murican, after all...).

@MattDMo Hmm... That would make sense, something that Watson picked up at Cambridge.... Also one of the co-authors, Jan A. Witkowski may be British as he was educated in England.

I found it in another context and would agree.  I don't see anything in the paragraph that would mean it had anything to do with the more common meaning of signalling.


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what is the biggest known functional distance between an enhancer and its target gene (TSS) in cis?
since the title seems self explanatory;
It would be nice if anybody could provide a reference. I'm looking for a paper that I belive stated around 1.5 Mb but anything above will be cordialy welcomed.
thanks a lot

I haven't found 1.5 Mb, but 1 Megabase. This is the case for the shh gene in chicken, where the enhancer element is located 1 Mb upstream. The original article can be found here:

"A long-range Shh enhancer regulates expression in the developing
limb and fin and is associated with preaxial polydactyly."

There are two reviews which are also interesting in this context:

When needles look like hay: How to find tissue-specific enhancers in
model organism genomes
Remote control of gene expression.

thanks. I also have encountered 1 Mb and distances slightly above, but I'm specifically interested in the longest known functional distance in cis. it is not as easy as I thought since I have spend now several hours on ncbi/pubmed ...

I can have an additional look later today. Do you have any idea in which organism or for which gene this has been described?

unfortunately i don't. i may belive belive it was in M.m - but then again if I remembered properly I would have found it by now. thanks again anyway

this paper "Extensive Promoter-Centered Chromatin Interactions Provide a Topological Basis for Transcription Regulation" at least states finding interaction-distances in the range of megabases... and leaves it at that.

I stumbled upon a few of these claims but they never show data or have references for it.

i found "On a chromosome far, far away"  and " Extensive promoter-
centered chromatin interactions provide a topological basis for transcription regulation.
". one of the papers claimed multiple Mbp and the other stated a range of 2-3Mbp. they did provide their 'not-fully-raw' data bu I have not yet calculated myself. anyhow, since it was I think you who recomended at least one of these two papers in another forum (what are the chances) I thank you


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Braquio-abduction illusion explanation and references
Illusion: Lying down on a hard flat floor move arms up and down (as when doing a snow angel) while keeping them touching the floor. While repeating it a few times the floor begins to appear concave, with the deepest part where the arms as perpendicular to the rest of the body.
Questions: What is the origin of this illusion?
My guess: I think it might be related to the arms being harder to extend towards the back when they are perpendicular to the body than when they are at other angles.
Note: The name above is only the way I like to call it. I found this illusion when I was a kid, but I am sure others might have noticed it as well.

It may be because, when we move our shoulders towards our the body, also know as abduction (Fig 1.) gives the central part of the body an elevation. when we rotate our arms more upwards (Adduction), the elevation will be lost.
So in other words, when we are making snow angels,

Start Normal position (hands near thighs) = Back and shoulders on ground
Middle position      (hands in middle)   = Back elevated and shoulders on ground
Final Position        (hands upward) = Back and shoulders on ground again.

Due to this motion, it seems as if the ground become concave.

Source:
Anatomical Terms of Movement
Articulating the Importance of Joints in Anatomy


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DNA barcoding, querry regarding tree based (cluster) methods for species identification
I am working on success rate of DNA barcoding in identification of species using distance and tree based methods.
Regarding distance based method, I have used Adhoc and species identifier and confirmed species identification using best closest match criteria (BCM).
Please suggest program/software/method for tree based identification (using NJ, parsimony, bayes), exhibiting clustering (number of clusters formed for particular species) that will suggest singleton (=Ambigious) species.
(For more details: Attached image)
(Please Note: It is not possible to do it manually as iam having >4000 specimens)
Answers detailing methods or softwares appereciated! Thank you!

Are you searching for something like this: http://en.wikipedia.org/wiki/List_of_phylogenetics_software
this post is some what off topic.

@Devashish Das, thank you for your reply, to make it more clear, ive attached image. Pls have a look, keep posting.

You can try PHYLIP and ClustalW. You can run them from commandline and this can be automated.


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Schedules of mating for men

It’s simple deductive logic to follow that for a species to survive it must provide it’s offspring with the best possible conditions to ensure it’s survival – either that or to reproduce in such quantity that it ensures survival. The obvious application of this for women is sharing parental investment with the best possible mate her own genetics allow her to attract and who can provide long term security for her and any potential offspring.
Thus women are biologically, psychologically and sociologically the filters of their own reproduction, where as men’s reproductive methodology is to scatter as much of his genetic material as humanly possible to the widest available quantity of sexually available females. He of course has his own criteria for mating selection and determining the best genetic pairing for his reproduction. This is evidenced in our own hormonal biology; men possess between 12 and 17 times the amount of testosterone (the primary hormone in sexual arousal) women do and women produce substantially more estrogen (instrumental in sexual caution) and oxytocin (fostering feelings of security and nurturing) than men.

From a biological point of view, is the bold sentence correct? And is the quantity of hormonal differences the only explanation of this?
Link to article: http://therationalmale.com/2011/08/23/schedules-of-mating/

Edit question and add a link to the cited paragraph!

Females are defined as the sex that produces that bigger gamete (ovule) while the males are those from the gender that produce the smaller gametes (spermatozoid). Because producing big gametes is costly, the number of females fix the reproductive limit in the population and in other words the variance in reproductive success in males is higher than in females. In the same logic, because females fix the reproductive limit in the population, males have to compete to access the females while the females are choosy. You may want to have a look at the wikipedia articles for Bateman's principle and Parental Investment.
The conclusions of Bateman's principle holds in general but not systematically. In some species males produce huge amount of parental care and therefore, the females become choosy for example.

[..] men’s reproductive methodology is to scatter as much of his genetic material as humanly possible to the widest available quantity of sexually available females.

Yes, in many cases but not everytime. Human are an example of the cases where this statement is wrong.

[..] for a species to survive it must provide it’s offspring with the best possible conditions to ensure it’s survival – either that or to reproduce in such quantity that it ensures survival.

It sounds a bit weird! The reason is that the sentence almost implies that individual's strategy evolved in order to increase the probability of survival of the species which is totally wrong. By the mechanisms of natural selection a population evolve in the direction so that each individual favors its number of offsprings which can be in some cases very detrimental to the species as a whole.
Reading some bits of what I found no the webpage you linked i your question, it doesn't seem to me that the author is a good evolutionary biologist…but I haven't read much.

Good post remi, Bateman's principle and parental care was worth looking into. I think the article present the theories in a very simplified "layman" terms. Some malformulated statements(like your last comment observed) but overall I see no fallacies.


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Identify a copper fuzzy moth
Photographed in 2003 in Panama. Not sure of size.

Its a relative of dirphia horcana and dirphia brevifurca

Cerodirphia avenata, a moth of the Saturniidae family. An anonymous person identified it. The person did not give any evidence, and I know nothing about moths, but its seemingly-distinctive wing markings wing frontal edges, and antennae match this example image on wikipedia and those I can see on iNaturalist also made in Panama.

Thank you for posting the answer you found elsewhere. Please note that you are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that support this conclusion and supporting references or at least validated images. Without this post is indistinguishable from opinion and thus is not appropriate as an answer on this site. ——— You may also wish to take the [tour] and then consult the [help] pages for additional advice on [Ask] and [Answer] effectively on this site.

thanks, I've added a (quite likely naive) justification


text:
What are the factors that control the speed of propagation of neuronal signals?
If we consider an analogy between a wire and a neuron there may be some resemblance between the factors controlling the data flow rate. For example the increased width of wire leads to decreased resistance etc; similarly increasing or decreasing the thickness of myelin sheath may have an effect on the conductivity or data transfer between neurons.
Are there additional factors that can control the speed of nervous conduction?

Are you interesting in processing speed (could be measured via reaction time for example) or in speed of signal transfer?

I think both are related to each other?arn't they.I mean one effects the other.My interest is in processing speed and yes/obviously it could be measured with reaction time but i was was interested what make's this speed at the cellular level

In this case look at synaptic delay. In my best knowledge it's the most time consuming factor of nervous conduction

Unfortunately, we cannot consider an analogy between a neuron and a wire; they are altogether different. Do you want to ask about the processing power of the brain, or speed of signal along a neuron? I suggest you pick one, and revise your question accordingly - unlike in electronics, these are quite separate concerns.

Well you are right i am interested in processing power of brain and i thought speed signal along a neuron will be involved in that matter.I think its to late for me to revise.

The diameter of axons also makes a difference, the thicker the axon, the faster the rate of action potential conduction. This is seen in invertebrates, such as squid. Squid have giant axons (up to 2mm in diameter), which exhibit rapid conduction rates. See Wikipedia 'squid giant axon', in which it says up to 1mm, but I have measured 2mm myself. These are not found in mammals.
Original research on squid giant axon  was by Cole & Curtis (The Journal of general physiology, 1939). For more recent research see Hartline & Colman (Curr Biol. 2007 Jan 9;17(1):R29-35.).
Work by Hodgkin, Huxley and Katz (The Journal of physiology, 1952,  116(4): 424–448) using squid giant axons lead to the elucidation of the mechanism of action potential conduction and a Nobel prize. Academic summary here: http://jp.physoc.org/content/538/1/2.full
Wikipedia: see the Goldman equation (Goldman shared the Nobel Prize with Hodgkins and Katz). This is more frequently known as the Goldman-Hodgkin-Katz  equation in UK publications.

The myelin sheath of a neuron affects conduction of action potentials.
Things to read through at wikipedia for example are the Nodes of Ranvier, the saltatory conduction and the Schwann cells.
There might be other features changing nervous conduction, but those are the ones I remember from my study times.

The question already includes the case of myelination.

It included also the words "may have". I just pointed out that this assumption is true. And the question only mentioned thickness, not gaps.


text:
Which turtle species was on board the Iranian Space Agency launch in 2010?
They are seen briefly in this video:
https://www.youtube.com/watch?v=nZoNdf6hlII
The launch made international news, but there was no mention of the species.
Here's the entirety of Wikipedia's description of the launch:

On February 3, 2010, ISA launched a Kavoshgar-3 (Explorer-3) rocket with one rodent, two turtles, and several worms into sub-orbital space and returned them to Earth alive. The rocket was enabled to transfer electronic data and live footage back to Earth. The Iranian Aerospace Organization (IAO) showed live video transmission of mini-environmental lab to enable further studies on the biological capsule. This was the first biological payload launched by Iran. Iran is the sixth country to send animals in space.

The Farsi language Wikipedia entry on the launch (کاوشگر ۳) does not appear to contain any more information on the species.
I've tried searching Google Scholar for papers, but my search turned up nothing. I also tried asking Reddit on the day of the launch, also without results.
Bounty Note: I appreciate all answers, especially from herpetologists. However, the bounty will only be awarded only for a reliable, third-party, published source (i.e. acceptable for use on Wikipedia).

We had this question here a while ago, it seems to be deleted. I looked for an answer back then and I wasn'T able to find one, so it has probably never been published.

Thanks for looking. It was deleted shortly after posting because it was cross-posted to Space (after a suggestion here), and then apparently you're not allowed cross-posting so the Biology one was deleted. It was only here for a short time. But it seems they couldn't find an answer so it's been sent back.

I apologize for the skepticism, but is there any indication this was a real turtle?

Can you try posting this on Skeptics SE?

Sorry, too big for comment!
It's actually hard to tell, as there is no official claim on this one.

Photo Link: http://youtu.be/nZoNdf6hlII?t=17s
Al I guess is, it can be:

Native breed of Iran like, Spur-Thighed Tortoise (Testudo graeca)

or something like this

(source: deserttortoise.org)
Trachemys scripta elegans


text:
Does Pseudomonas aeruginosa have any common name at all?
Pseudomonas aeruginosa is the fifth most written about¹ binomial name of all species. I'm having trouble coming to terms with the possibility that such a well researched and studied organism has never been given a shorter vernacular name. I can't find one listed anywhere.
Is there any short common name for it? Even a colloquial one? Maybe a pet name common to microbiologists or students in the labs of some particular region? I'm mostly interested in English but how about in other languages?
I am aware it can be abbreviated to P. aeruginosa. I don't consider that a common name. Pseudomonas by itself refers to a genus of around 191 species.

¹ "most written about" meaning mentioned in the most books or volumes of Google Books' English corpus (ngram data), according to my own research. The top five are: Homo sapiens, Escherichia coli, Staphylococcus aureus, Candida albicans, Pseudomonas aeruginosa.

Soil bacterium?

Not as far as I know. It's sometimes referred to as Pseudomonas alone, but not more.

Pythagoras is written about a lot in Philosophy and Mathematics, yet I've never seen a shortened version of his name. Some organisms do have shortened versions, e.g. C. diff. It works. I suspect P. aerug is clumsy to say. Pseudomonas is easy to say.

In medicine, it's often shortened to just "Pseudomonas", but that's about it.

That's odd because I've never heard Pythagoras the Samian, the mathematician, not the sculptor of the same name, referred to by anything but just his first name. Shortening to just the genus "Pseudomonas" might make sense in medicine where infections by other Pseudomonas species are rare (and perhaps treated similarly to P. aeruginosa?), but for microbiologists there are 190 other Pseudomonas species to distinguish between when referring to P. aeruginosa.

I can't think of any common names given to any bacterial species. Is there an example you can give?

Golden staph is the obvious one.

Well in that case, how about "rusty pseudo"…

Staph, Strep, H. flu, Toxo, there are a few more. But partly it depends on how easy it is to say. @Qubei - yes, there are a few other Pseudomonas species that can cause trouble, but P. aeruginosa is by far the most common; if it's a different species, we'd say the whole thing.

The rule for so-called common names seems to be to abbreviate the genus names. Straightforward yet ambiguous.

I think there's a difference between a vernacular or common name ("tiger", "cat", "pigeon", "elm", "pine") and a pet name or nickname as you use it here. The former are names in human languages for a particular kind of animal or plant, while the latter are a colloquial name used by professionals to refer to a particular species, often based on its scientific name.
I can't think of many micro-organisms that have a true vernacular name -- most micro-organisms were given fancy scientific names, and those were used consistently thereafter. The only proper microscopic common name I can think of is "slipper animalcules" -- but I'd be happy to be proved wrong!
Lots of micro-organisms have pet-names -- E. coli, C. diff., "smallpox", "Ebola", "white nose", even Pelagibacter ubique -- but they're either based on the scientific name or on the disease the organisms cause. AFAIK (and based on the comments), Pseudomonas aeruginosa doesn't have one. However, of the list of species you list, only H. sapiens has a vernacular name, while the others only have nicknames based on their scientific name, so I'm not sure it's that surprising! IMO it's mostly macro-organisms that get vernacular names.

Good distinction between vernacular and pet name/nickname, but in the end I am looking for either.


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What is the nature of these sprouts?
With zero knowledge of botany, but curious enough to do some research of what I observe, I would like to know the reason for this young sprout in the lower part of a 2 m long Hoya carnosa. I did not find this phenomenon after looking for it on the Internet.

It exhibits a different kind (shape, color, thickness, consistency...) of leaves, thinner and clearer stem, suction cups ... I've read about foliar heterophilia, sports, ... but these phenomena don't seem to explain what I observe. I've also thought about parasitic plants. Could you provide some insight into this?
EDITED (after digging a bit):
The roots are quite tangled, so it is difficult to identify if the wooden stem the sprout comes from is connected to the Hoya stems. If not, the creeper has managed to keep idle for ~5 years with no visible green parts.

That's a creeper of some sort (looks like Vitaceae family.) It cannot sprout naturally from your Hoya. Viruses and chance mutations can change some aspects (e.g. gall or coloration of leaves).  Mutations are called sports, as you mentioned. But nothing can turn a Hoya into a creeper. If I could examine the source carefully, I could tell you more, but the sprout probably came from the soil the hoya is planted in, or found purchase in part of the hoya (this is unlikely, as it would reach a limit of nutrients and die.) "Like produces like" in seed and within the plant itself.

@anongoodnurse I'm not sure what you mean by "the source". The sprout is inserted in the wood, which should be Hoya wood. And there seems to be no direct connection to the soil at that point, besides two thin "threads" that just fall on it. I added a 4th photo.

As I said, this cannot occur "naturally", i.e. the hoya cannot have given rise to the creeper. And, again, as I said, I would need to examine it more closely to determine what's going on here, and maybe a dissection would be in order. Wat you may be proposing requires part of the hoya to completely change its genetics, which it cannot do.

I guess the most probable reason for this is... the wooden part was already a creeper, which has been idle for at least 5 years.

Yep, looks like a completely different plant rooted in approx the same location as your Hoya. I don't think Hoya stem will ever look like that brown one.

Well, about appearance, it doesn't seem to me so different when compared to the right end Hoya stem at pictures 3rd and 4th.


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Could the growth rates of Vibrio vulnificus be affected by an oil spill?
I live on the Gulf Coast, and Vibrio vulnificus has recently made the news due to an increase in the number of reported infections. Naturally, it has people around here worried. I live in an area that was affected by the BP Deepwater Horizon oil spill, and many people are concerned that the oil or byproducts of the clean-up could be fueling the growth of this and other bacteria.
I know that bacterial species which are capable of metabolizing the components of crude oil exist, but are rare. I also know that Vibrio vulnificus thrives in warm salt water, and since it is a "flesh-eating" bacteria that infects shellfish, it must be capable of "eating" organic material.
I can think of several possibilities that might explain an increase in reported infections:

The amount of bacteria and the number of infections is actually the same, but reports have increased due to more awareness in the public and in the medical community.
Warmer water temperatures in the Gulf in recent years have led to more bacterial growth.
The bacteria is capable of metabolizing crude oil, its degradation products, or one of the other cleanup chemicals (Corexit, for example).
The oil spill has compromised the immune systems of the organisms that are typically V. vulnificus hosts, which has led to higher infection rates and therefore, more bacteria.

There could of course be other explanations, but these are the ones I came up with off the top of my head. I imagine that if bacterial populations actually have increased, then any of these scenarios that are possible would likely contribute something.
However, in the short amount of research I have done, I haven't been able to find any concrete data that shows whether populations have increased at all, or whether they could be affected by the oil spill.
My questions are:

Are there any studies that show the population of V. vulnificus over a time period covering the BP Horizon spill (this happened in April 2010, and oil products are still washing up on beaches in small amounts)
Is it possible that it could be metabolizing oil or other chemicals related to the spill?

Wikipedia says that the strain is common in the gulf of mexico. Probably the living conditions were better in the last time so the population got much larger.

My educated guess is that it's a little of one and two, a lot of four and things like four(decrease in biodiversity, lack of predation, habitat disruption, etc), and probably not 3. 3 would be a big deal, because it could revolutionize oil spill cleanup technology. Worth checking to see if it's happening, though.

I found these article, which show exponential increase in population of Vibrio in BP oil spill region (published in 2011 supported in 2013).$^{1,2}$
There is evidence that Vibrio representatives can metabolize oil-derived compounds $^{3,4}$. There is a sizable amount, more than 31%, where found in the Deepwater Horizon Spill.$^5$. Though the reason is still to be proved $in\ vitro$, but studies shows they can persist in the presence of oil.$^6$
Source:
[1]:
High Numbers of Vibrio vulniﬁcus in Tar Balls Collected from Oiled Areas of the North-Central Gulf of Mexico Following the 2010 BP Deepwater Horizon Oil Spill
[2]:
Associations and dynamics of Vibrionaceae in the environment, from the genus to the population level
[3]: West 1984, Numerical taxonomy of phenanthrene-degrading bacteria isolated from the Chesapeake Bay.
[4]: Moxley K., Schmidt S. (2010). Preliminary characterization of an estuarine, benzoate-utilizing Vibrio sp. isolated from Durban Harbour, South Africa. Curr. Res. Technol. Educ. Top. Appl. Microbiol. Microb. Biotechnol. 1249–1254
[5]: Hamdan L. J., Fulmer P. A. (2011). Effects of COREXIT® EC9500A on bacteria from a beach oiled by the Deepwater Horizon spill. Aquat. Microb. Ecol. 63, 101 10.3354/ame01482
[6]: In situ and in vitro impacts of the Deepwater Horizon oil spill on Vibrio parahaemolyticus.

These are all good articles - thank you. I don't agree that refs 1+2 show an increase in Vibrio outside of populations within the tarballs themselves, but since I can't find anything else to support/refute that idea, I am accepting this answer. Thanks again!