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What causes a tendinopathy to calcify?
I read in this 2012 research paper {1}:

The aetiopathogenesis of CT [calcific tendinopathy] is still controversial, but seems to be the result of an active cell-mediated process and a localized attempt of the tendon to compensate the original decreased stiffness.

Has the cause of calcific tendinopathy been more clearly determined since then?

References:

{1} Oliva, Francesco, Alessio Giai Via, and Nicola Maffulli. "Physiopathology of intratendinous calcific deposition." BMC medicine 10, no. 1 (2012): 95. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482552/ ; https://dx.doi.org/10.1186%2F1741-7015-10-95

The article that you linked states that the exact mechanism is not known but lists different theories. A question like "has anything more been discovered" is broad. Did you try checking the articles that cite this one? It's easy to do that on google scholar.

@WYSIWYG 109 articles cite this paper, and a paper that found the cause of calcification might not have cited this paper. I was hoping that some expert on this website already knows the answer. The question is clear and I don't think it is too broad: The question is "What causes a tendinopathy to calcify?" If that's too broad, you'll need more than 40 close votes per day.

The question "What causes a tendinopathy to calcify?" is broad indeed. There may be several processes involved at the subcellular and tissue level. It is not possible to list and explain every pathway involved. You must add more details to your question. You certainly know more than me about this field; you can look at more recent papers. The paper that you mention is the first hit on google. Since you study tendons you could definitely search more recent papers on this topic. You can add those findings and make your question more precise.

@WYSIWYG If the question "What causes a tendinopathy to calcify?" is closed as too broad, then a large portion of questions posted on https://biology.stackexchange.com should be closed for the same reason.

You can certainly vote to close them.

@WYSIWYG I don't think it's too broad, and I think one should cast close vote consistently across questions. https://biology.stackexchange.com/tour says "Biology Stack Exchange is a question and answer site for biology researchers, academics, and students". The question  "What causes a tendinopathy to calcify?" is perfectly fine for student-level.

I don't want to go into an extended discussion but just to make you realize I'll throw a similar question at you: what causes diabetes? Tell me if it is broad or not. Anyway, I think your question is broad and needs more details and I am free to vote my opinion.

@WYSIWYG Not all "What causes X" questions are equally broad. In the example you gave, diabetes is a group of diseases and many factors play a role. The aetiopathogenesis of calcific tendinopathy is much more narrow in scope. I think that inconsistent close vote decisions are deleterious for the website, since it means that questions might be closed subjectively and not according to clear rules.

@FranckDernoncourt I agree with WYSIWYG. The problem is that if the answer is "Nope" it is impossible for someone to find a reference actually answering that. If the answer is "No, but X has found 1), Y has found 2), and Z has found 3)" since 2012, you've basically had someone write you a new review article; they should publish it instead of posting here. Only in the circumstance that there is a new canonical review that you are not aware of but exists as one of the 100 citations for that paper is there a sufficiently narrow answer for someone to post.

@BryanKrause "Only in the circumstance that there is a new canonical review that you are not aware [...] there a sufficiently narrow answer for someone to post" -> yes this is what I am looking for and this is why I wrote "Has the cause of calcific tendinopathy been more clearly determined since then?" in the question.

@FranckDernoncourt The best advice I ever got in grad school was from a senior grad student at the time passing on advice he got from his advisor. She cautioned him to study questions where the outcome is interesting no matter what, to avoid getting stuck in a place where you have an answer but it doesn't mean anything. Similarly, a SE question that is probably unanswerable is not a good question: it ends up either with a bad answer or it lingers as a bad unanswered question.

@BryanKrause Then your close vote reason is different from  WYSIWYG. If your reason is that "SE question that is probably unanswerable is", then 1) the study I mentioned is seven-year-old, science has progressed since then and there might be a clear answer by now 2) if experts in the field are aware that the question currently doesn't have any satisfying answer, then that's an answer in itself.

@FranckDernoncourt No, I think the reason is the same: either it requires a too-broad answer, or it is not answerable, therefore it is too broad. I think the probability of "Only in the circumstance..." is sufficiently low to ignore entirely.

@BryanKrause How do you view "not answerable" as "too broad"? One example of answer is "study X published in 2018 showed that aetiopathogenesis of  calcific tendinopathy is Y". Another example of answer is "study Z published in 2019 indicates that no consensus has been found so far" etc. The question is perfectly answerable.

@FranckDernoncourt I disagree and I've already explained why. I won't argue this further here.

@BryanKrause the question is perfectly answerable as my previous comment illustrates


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Why does it take 24 hours for tendons to give feedback on whether the loads they received were excessive?
I heard in this interview of Jill Cook (tendon researcher) on https://youtu.be/GKkSp-TlofI?t=230:

Tendons talk to you 24 hours later. So what happens if if I put load on a tendon today, it will tell me tomorrow it's been happy with the load.

Why does it take 24 hours for tendons to give feedback on whether the loads they received were excessive?

In this article, they say that they believe any pain that lasts more than 24h during rehabilitation should be considered a contraindication. No reference was cited for this reasoning. I believe it takes 24h for recovery. My suggestion is that you write to the author herself asking for the relevant reference. You can then post that as an answer. It is unlikely that you would receive an answer here because this is a very specialized topic.

It sounds like the person in the interview was referring to delayed onset muscle soreness, of which there is an interesting wikipedia article

source: Stack Exchange

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sort: votes


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Is it possible to detect whether an organism has been gene edited (by humans)?
Is it possible to detect whether an organism has been gene edited? For example, if someone gene-edits a human embryo (e.g., as He Jiankui did last year), can one later detect whether the human has been gene-edited?

This is largely going to depend on what is changed. Gene editing can cover a wide range of things.

If you had access to the DNA of the organism's parent(s) then you could make an inference about whether the child's genome is consistent with being edited, assuming that the edit was done early enough in the embryo's existence for the edit to be present in all/most of its cells. If the organism is a chimera/mosaic, then it may be possible to detect the edit by comparing different tissues within the organism, and identifying differences which do not look like 'natural' somatic mutations.  However, I don't think we have a good handle yet on what the natural range of somatic mutations looks like, so it might be difficult to assess whether any difference found were of an engineered origin.

I think you're last point is very important - depending on the type of change introduced (and the technique used) it could look like a single point mutation or other minor changes that are indistinguishable from natural chance events.

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Can lymph be in peripheral blood?
I read an argument that 1-3% of lymph is in peripheral blood.
However, I am not sure if this lymph is about lymphocytes in peripheral blood; not lymph itself.
Lymph gets exchanged between capillaries through Starling law powered by the heart and Frank-Starling mechanism.
In this way, it makes sense that some lymph is leaking out from capillaries into the bolod.
Can lymph be in the peripheral blood?

Depends if your talking about interstitial fluid or lymph:
As per starling forces: the oncotic pressure of the late capillary plus hydrostatic pressure of interstitial space, would be higher than oncotic pressure of interstitium [though I dunno why since intertitial GAGs are very water hungry and they are responsible for the negative (hydrostatic?) pressures found in interstitium... Read lots of articles, still makes no sense to me] and hydrostatic pressure of the capillary... Thus there would be a net influx of interstitial fluid in the very ending part of the capillary, toward the venous side...
I say interstitial fluid, because it's not lymph yet since the interstitial fluid hasn't yet entered the adjacent lymph capillaries... if the interstitial fluid entered the lymph capillary then it would be stuck there, the mechanism of this one way flow is the junctions between the endothelial cells in these blind ended lymph capillary... These junctions which only opens up gaps between these endothelial cells when the interstitial pressure outside the lymph capillaries is higher than pressure inside the lymph capillaries...
The lymph then goes forward through lymphatic vessels/nodes because external pressure (pulsing of adjacent artery, contraction of adjacent skeletal muscle, changes in thoracic pressuring during breathing, etc) and there is little back flow because of valves (just like venous valves which prevent back flow in the low pressure venous system)... Ultimately the lymph returns by either thoracic duct (in the angle between left subclavian and left jugular vein) or right lymphatic duct  (in the angle between right subclavian and right jugular vein)...
There are some sweet review articles from University of Bergen, Norway that go much more in depth on the physiology of interstitial fluid...
Here is one of their more recent review articles:
http://m.physrev.physiology.org/content/92/3/1005 it's free
IN SUMMARY: the starling forces bring interstitial fluid into the blood (the "peripheral part" right after the capillary)... The thoracic and right lymphatic duct drain lymph into the blood (I'm assuming this does not apply by your definition of peripheral, since this venous blood is about to be drained into the right atrium and is destined for the lungs)...
P.S. aqueous humor (in the eye), endolymph (cochlea aka inner ear) and CSF are also absorbed back into the blood... Also the brain has an interstitial fluid that is different from the CSF found in the subarachnoid spce of the meninges, i actually don't know how that drains... But anyway, the head is so special, I'm sure you weren't wondering about these specifics...

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text:
What is the difference between fibrogenesis and fibrosis?
Fibrosis is the formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process.
I used the word "fibrogenesis" as the outcome of acute inflammation (healing).
My colleges use the word "fibrosis".
The fibrogenesis seems to be used with the emphasises of the genetic part.
What is the difference between fibrogenesis and fibrosis?

As a note, the suffix -genesis refers to the development or production of something, while the suffix -osis can be roughly translated as '...a current state of...' something.

I would say fibrosis represents an abnormal accumulation of fibrous tissue usually collagen fibres. Where as fibrogenesis is the process of formation of fibrous tissues be it collagen, reticulin, elastic, oxytalan..

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can a protein recognized by antibodies not be immunogenic?
I have a protein that is produced with the baculovirus system that is recognized by antibodies generated by immunization of rabbits with the same protein produced in E. coli. However the baculovirus protein did not induce an antibody response when I immunized some pigs.
Could it be that the baculovirus protein is not immunogenic? Even if the same protein is recognized by antibodies? If the rabbits produced antibodies with a protein that did not have post-translational modifications, how can not be immunogenic when the modifications are added?

What kind of protein is this? A protein from pigs? Or one which is at least a highly homologous with a pig protein?

Did you add some special tags in your bacterial expression system? It is possible that the original baculovirus protein does not elicit immune reaction because it mimics a host protein. Many viruses use this strategy to evade immune response. The bacteria-expressed protein may have folded differently leading to the loss of the molecular mimicry.

it is a viral protein. I infected rabbits with the E. coli version and I got an immune response; the baculovirus version instead did not elicit a response in pigs. I used adjuvants to infects pigs

Pure proteins are often poorly immunogenic because you need to have some kind of "adjuvant" effect to induce a strong effect. Bacterially-produced proteins may well have some bacterial LPS or other immune stimulants still present after purification which would drive a much stronger response than the same protein produced from eukaryotic cells. There are many other possible explanations -- one or the other protein may have aggregated or misfolded, which could drive a different response, for example.
In other words the effect you're seeing may be annoying but is not particularly shocking, and you have no choice but to do some routine troubleshooting at this point. Is your protein more immunogenic when administered with an adjuvant? Are the two versions identically folded? Are there antibodies present to a misfolded form that you're not detecting? And so on.

Thanks, different folding was also my guess. I did not consider the LPS residual though.

@Gigiux If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered. If you have >= 15 reputation points, you may also upvote the answer if you wish. There is no obligation to do either.


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Evolution to store limited Fat
Why are our bodies not evolved to store only limited amounts of fat, which won't kill us with all diseases associated with obesity?
Wouldn't obese people die faster and clean the gene pool for people who are slim?

Guess-work here! Probably because disease related to excess of fat is a very modern thing. I would guess that being able to store fat was highly selected for survival but maybe also for reproduction (fat and sexy). Note also, that we stop eating after a while. We don't eat until we die suggesting some defence mechanism here.

Search for thrifty gene hypothesis.

For some organisms, being gluttonous and storing fat is an optimal survival strategy which is linked to their foraging/hunting strategy. I would guess that for an early human with a hunter-gatherer lifestyle, being gluttonous and storing fat would have been useful. This is not suitable for our current lifestyles. There are some animals that have a tendency to become obese, when in captivity (and overfed).

Worth remembering that if you're physically active and products like refined sugar aren't available it's actually quite difficult to get obese, and things which don't happen can't get selected against.

"Wouldn't obese people die faster and clean the gene pool for people who are slim?" Not before reproducing. By your logic, look around you. Do you see a whole lot of skinny people, or do you see a fair amount of obesity? What does that tell you?

For most of human history the excess of food has not been a problem, rather the lack of food, and subsequent starvation has been a problem. So genes that promote energy efficiency and fat storage have been  very much selected in the human population. So much so, that humans are rather fat for apes.
As for the problem of obesity, it has been a rather recent problem, no more than one or two generation. Evolution works in generation time. So there is not enough time to weed out genes that promote obesity which would be pretty common in human gene pool.

Human the fat ape http://www.sciencemag.org/news/2015/06/why-humans-are-fat-primate

Famine is really common in human history. So the ability to survive one is really useful https://en.wikipedia.org/wiki/List_of_famines

"Wouldn't obese people die faster and clean the gene pool for people who are slim?"
If your hypothesis is right, the selection for such traits would only have begun in the last 20-30 years ("Worldwide obesity has more than doubled since 1980" http://www.who.int/mediacentre/factsheets/fs311/en/)
Natural selection wouldn't have had time to select against people showing tendency for obesity.
Also, obesity is a lifestyle choice, and not merely predictable by genetic disposition. I could be a "fit" person, but genetically predisposed to obesity.
Look up also genotype vs phenotype for further reading (http://evolution.berkeley.edu/evolibrary/article/genovspheno_01)

It's very complicated to know how a trait would have been selected for or against in the ancestral environment. Tendency to gain weight does seem to have been selected for in some populations - e.g. pacific islanders. Presumably the decreased chance of dying from starvation was enough to compensate for any increased risk of heart disease, if in fact health risks did exist. Morbid obesity as we know it today may simply not have been possible without the modern diet, and modern society/technology to provide an endless supply of easy to reach, unhealthy, addictive food.

This is an interesting question, and shows good insights in trying to glean cause and effect of large social phenomena. However, the natural selection process as presented in your question has a couple issues.
Primarily, natural selection is a passive process. The concept that we developed those traits we "need" is a misrepresentation of the process. It is more accurate to say we adapt to take advantage of what we have developed.
I.e. Fish don't grow lungs because they want to go on land. Transitional fish go on land only if they happen to have lungs. If it gives them a fortunate advantage, then reproduction may expand the population of that attribute.
There is also the issue that obesity does not cull the population before reproduction in most cases. The effect you're expecting is less impactful then you assume in the OP.


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Quantity of toxin release by pathogen in host
I came across these lines from this paper:

Pathogenic microbes exert a broader sphere of influence by releasing a bolus of toxin that can act upon many cells within a given tissue and/or diffuse away to modulate one or more types of cells at multiple locations within the host.

What does this line mean? Does it mean that the pathogen releases multiple types of toxins or does it mean that the pathogen releases just one type of toxin in a large quantity?

bolus: MEDICINE - a single dose of a drug or other medicinal preparation given all at once.

@MattDMo I want to know what the sentence mean from the view of the pathogen

As I commented, a bolus is a single (often large) dose of a drug or compound given (released) all at once. Please read the very next sentence after the one you quoted:

For example, the lethal and edema toxins of Bacillus anthracis disseminate within the host bloodstream and act upon both immune and nonimmune cells.

This gives an example of a pathogen releasing multiple toxins, although there are other pathogens such as Clostridium tetani which release a bolus that consists of only one toxin. So, it can be one or the other.


text:
Using exogenous genes to reduce the set of essential amino acids?
Various organisms have sets of essential amino acids that they cannot synthesize themselves, but rather that they must obtain from food. Humans have 9 of these amino acids. However, obviously certain organisms like plants contain the necessary genes to synthesize all of their amino acids. Also, the set of amino acids for various organisms differs. For example, arginine is essential in dogs but not in humans.
Have there been any attempts at taking cells from an animal or other organism with essential amino acids and providing them with the necessary genes to synthesize that amino acid, thereby reducing the cell's set of essential amino acids?
I am not asking this specifically referring to human cells, nor do I have any particular motivation for asking this other than curiosity.

Decreasing the number of essential amino acids is frequently used as a selection marker during molecular biology experiments: An organism (usually yeast) that cannot synthesize a certain amino acid is first grown in the presence of said amino acid in the media. Then it is transfected with a gene of interest together with the gene that enables it to synthesize the amino acid. Now being grown in a culture medium that does not contain the amino acid, only individuals that were successfully transfected can grow, the others will starve.
A similar approach was also used in  Beadle and Tatum's Nobel prize-winning work on the one gene-one enzyme hypothesis.


text:
immunity to Malaria
What is "immunity to the disease" in the following sentence?

In some regions, the parasites are resistant to certain antimalarial drugs, particularly chloroquine.
  People continually infected gradually develop immunity to Malaria.

where does that come from? can you give a reference? Is the text "People continually infected develop immunity to Malaria" directly from a source? Is there supposed to be some punctuation somewhere?

When there is one existing subclinical infection, it prevents another new superinfection. This is called premunity and is rather very important for malaria inendemic areas. Just thought of mentioning. Its different from the immunity you're talking of though.

I would think it is not immunity to the Plasmodium, but rather something like a system-free infection. They don't get the symptoms of Malaria any more, but they are still infected.

They might build up slowly an immune response to the manifestation of symptoms of malaria that arise when the microorganism is present in the blood, from what I remember. But can't get rid of it since it hides when not in the blood (cycles in the liver if I remember correctly.


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Function of human kidneys
Why are the kidneys called metanephric? What does the term metanephric actually mean? I tried to search that on Google but couldn't find the exact meaning.

Start with mammalian kidney development: http://www.els.net/WileyCDA/ElsArticle/refId-a0001152.html

There are metanephric diseases, which refer to the location of pathologic tissue relative to the main kidney mass, but unless someone with more expertise wants to weigh in, I don't think that kidneys themselves are called metanephric.
There is also a developmental stage of the kidneys, in which they are referred to as metanephros. Perhaps you're thinking of that?


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Do different emotions produce different tears?
Do tears of joy, laugh, grieve, and others contain different things or are they all the same?

Basal tears

are always in our eyes to serve the purpose of lubricating, nourishing, and protecting the eyes.

Reflex tears

protect the eyes from irritants, including wind, smoke, or onions.

Tears produced by emotion

Although these tears contain higher levels of stress, such as ACTH and enkephalin, and endorphin and natural pain killer, they can also work by directly calming the iris down while signaling the emotional state to others.

Secretion of tears

The lacrimal gland, located in the outer part of the upper eye, is constantly secreting a protein-rich, antibacterial liquid. This fluid goes from the outer edge of the eyeball toward the cornea and lubricates the entire eye surface every time we blink.

Sources:

http://archopht.jamanetwork.com/article.aspx?articleid=625096
http://www.sciencedirect.com/science/article/pii/0002939481906516

Could please post the references to all these claims. Without the references, these are just sentences.

Please cite references that are either peer-reviewed publications, books, educational/informational websites hosted by reputed agencies (universities/research institutes/educational foundations) or even a well curated wikipedia (other encyclopaedia) article. I personally do not consider science blogs as valid references, especially if they are written by non-experts, for non-experts. They are often exaggerated and lack cross references.

@WYSIWYG I agree, I'll add a "good" reference later when I get home


text:
How does hypocalcaemia have an effect on the excitability of cell
Hypocalcemia increases sodium influx by leak channels. Why does this elevate the resting membrane potential and increase excitability?

Which cells are you talking about? Where did you obtain the information from?

Assuming the question is in respect to neurons..in a nutshell...resting membrane potential & excitability both depend upon sodium permeability which in turn depends on potential difference of the excitable cell....now as the sodium influx is increased the minimum voltage required to increase the conductance of sodium decreases far below its normal value...so for a small increase in membrane potential from the normal very negative level the sodium channel becomes activated elevating the resting membrane potential...
In fact, the calcium ion concentration needs to fall only 50% below normal level before spontaneous discharge of peripheral nerves occur giving rise to "tetany"...
Reference- Adapted from Guyton & Hall- Textbook of medical physiology (12E)
You can also refer to Berne & Levy's & Ganong's physiology book for further details


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How to characterise a protein family in a putative genome island?
We have sequenced the genome of 200 bacterial strains belonging to the same species, a swine bacterial pathogen. In a previous work, it was observed that a protein family of adhesins is present in some of these strains. Each strain has multiple copies separated in their genome. Genetic differences have been observed among the DNA sequence in the different strains. Since some mobile genetic elements are present near these genes, it is possible that they are playing a role in the molecular evolution of this protein family.
How could I add additional evidences that this is a putative genomic island?
Some references would be also appreciated.
Thanks
UPDATE: For each strain, I thought about extracting the genomic region were these genes are located, maybe 8 Kb up- and down-stream of the gene. Then, running a miriad of tools to try to predict some of these island-associated elements. However, assuming that these "sequence-based" tools need the entire genome sequence, is it possible that I run them using the whole genome sequence and then focus on certain selected genomic regions?

Check this. You might find tools you are looking for. For second question, you can do cheap trick by just separate your area of interest from your whole genome and then feed that sequence as single genome into tool again.


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What is the conical mouthpart of a soldier termite and what does it do?
I'm trying to get a visual understanding of termite anatomy and I'm getting quite confused on the protruding mouthpart area (it looks like a beak) located between the pincers.
What does it do / what is it for? It does not look like a chewing mouthpart.
Further, is it related to the mouthparts of the worker / females termites?
Oddly enough, I found "Conehead" termites with what appears to be a far more profound version of this part (though it might not be) and again I see no purpose for it.
Is there a place on the internet where the breakdown of termites can be found? This would be very useful.

What is between the pincers?

This is actually the termite's labrum. Its quite big in termites. Does not have value in telling male from female.

Hi Jules~verne. We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. Answers that don't include explanations may be removed. Please update. Thanks! :)


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Genetics problem, test-crossed

Image description: text reads "An $F_1$ x $F_1$ self gives a 15:1 phenotypic ratio in the F2. What phenotypic ratio would you expect if you test-crossed the F1?"
How do I find out the $F_1$ phenotypic ratio by using the given $F_2$ phenotypic ratio?
What method should I use to solve?

Please show an attempt at solving this question or it may be closed.

Test-crossed f1 : AaBb X aabb
AaBb:1/4
Aabb:1/4
aaBb:1/4
aabb:1/4
ratio is 1:1:1:1

I have no idea what should i do next

PLEASE DO NOT POST TEXT AS IMAGES. Copy and paste the text into your question. Images are not searchable, and can not be interpreted by screen readers for those with visual impairments. Use the [edit] link to modify your question. See this for more information.

The 15:1 phenotypic ratio resulting from the self cross suggests duplicate dominant genes without cumulative effect.
In other words, two genes with complete dominance and dominant alleles producing the same phenotype, but independently, meaning that dominance at one locus ~ dominance at the other locus ~ dominance at both loci as far as phenotype is concerned.
So, in the self cross:
AaBb x AaBb =>
9 A_B_  double dominance = dominance
3 A_bb dominance from A
3 aaB_ dominance from B
1 aabb recessive
So that's where you get your 15:1 dominant:recessive phenotypic ratio.
Now, with a testcross, you were on the right track:
AaBb x aabb =>
1 AaBb
1 Aabb
1 aaBb
1 aabb
So, comparing this to the selfing results above, you'd get 3 dominant : 1 recessive for your phenotypic ratio.

Let me know if this answers your question!


text:
Optimizing Gel Electrophoresis: Ampere, Volts and Buffer concentrations
I am a master student in biochemistry, and I have used gel electrophoresis many times before. What I want to know is how one should adjust the mA (mAmpere) compared to the voltage and the buffer one uses.
Normally I used 1xTAE buffer (run at 90V) or 1x sodium borate buffer (run at 110V). I know that if I adjust the voltage up, the buffer heats up faster, the samples travel faster, but the "picture" of the gel becomes more blurry. This is however all I know about adjust the parameter.
So my questions can be summarized as the following:

How should I adjust the ampere, is there a range I should be in
compared to the buffer or sample I am running?
Does the ampere effect the travel speed if adjusted up or down?
Can I adjust the concentration of the buffer to run sample at a
higher voltage, what effects will this have (to increase or decrease
concentration)?
Is there a relationship between the ampere and the voltage which I
can manipulate, in this case: how and why?

This page by Thermofisher also gives a lot of tips for optimization: https://www.thermofisher.com/se/en/home/life-science/pcr/elevate-pcr-research/agarose-content-with-tips-and-tricks.html

As far as I know you can either adjust the ampere or the voltage as
both is dependent of the resistance from the buffer. Which means that
I would suggest you to let the voltage as it is.
As the ampere = voltage / resistance and voltage = resistance *
ampere and as you can see that the voltage has to get higher if the
ampere is increased and the ampere has to get higher if the voltage
is increased (at least if I understand it correctly) the travel speed
should be increased the higher the ampere is set.
I would neither decrease nor increase the concentration of the buffer. Maybe easily using another kind of buffer would help you. But this depends on the different samples you are running. Maybe that could help you:
Brody, J.R., and Kern, S.E. (2004). History and principles of conductive media for standard DNA electrophoresis. Analytical Biochemistry 333, 1–13.
The resistance is more or less given. Therefore as far as I know: No.


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Are alleles equally sized?
If alleles occur at the same locus on a chromosome, does that mean they are of the same size? I was under the impression that they were, but I saw a gel electrophoresis testing different alleles of the same gene and saw them separate. I don’t understand how they could separate if they are of the same size, but if they aren’t, then how can they be housed in the exact same locus?

Are you sure it is just a normal gel electrophoresis? It could be some technique like RFLP which can differentiate alleles.

If they are not on the same locus, then you can find them using electrophoresis. Basically you are checking for copy number. However, alleles at same locus can be of different sizes (but I don't think the differences are that great, in most cases). There are a lot of possibilities but unless you provide details, it is hard to explain what exactly you observed in your experiment.

In general, alleles don't have to be the same size. Two major examples which come to mind are the Huntingtin gene and FMR1.
Huntingtin is the causative gene of Huntington's disease. In people with Huntington's, a sequence of three nucleotides is repeated. The number of repeats varies, from a low of 9 in unaffected individuals, to more than 60 in severely affected ones. So depending on how many repeats you have, each of your Huntingtin alleles may have a different nucleotide size.
FMR1 is the causitive agent of Fragile X syndrome. Like Huntingtons, the gene varies in the number of trinucleotide repeats, but for FMR1, affected individuals can have over 1000 repeasts, meaning an extra 3 kilobases of genetic material versus the alleles of an unaffected individual.
Other genetic disorders are also related to the difference in allele size. You can have a deletion of a region of DNA (or an insertion) which is normally silent (recessive). The normal-length allele compensates for the defective allele, but the differently-sized disease allele is still present in the population, and counts as an allele of the gene.
It's not just disease-prone alleles which exhibit length polymorphism. A number of other genes will show variation on both the DNA and on the protein level. If the insertion/deletion is a multiple of three nucleotides and occurs in a loop region of the protein or on an intrinsically disordered domain, the insertion has a reasonable chance of minimal structural effect on the expressed protein. For one (completely arbitrary) example, PER3 has two major length variants in the population, with a 54 base pair difference between the two. Different populations have vastly different prevalence for each, with a range of 20-90% for the shorter version.
One thing to keep in mind is that "locus" points are just a human convention to help us map DNA. To the cell, DNA is just a single long molecule. (Or multiple molecules, for different chromosomes.) There isn't any labels for absolute position in the cell, so inserting or deleting a chunk of DNA mainly affects just the local environment. There isn't any sort of long-range indexing that gets messed up by the insertion.

So what exactly happens when the repeats increase? Does this gene code for a specific enzyme? Do the increased repeats change the enzyme activity?

@curious_cat the exact function of huntingtin is not really known. In most of these poly-Q proteins, the repeat is not present in any functional (binding/catalytic) regions. This ideally should not affect their activity but there are other factors at play here. The exact mechanisms of poly-Q toxicity are still not clear: one thing that is known is that this causes a stress response.

@WYSIWYG What about in general? Say alleles that determine other phenotypic features, say eye color or sickle cell anemia or hemophilia etc. How do the difference in amino acid repeats / type lead to the feature difference. What is the mechanism. Is it a specific enzyme's activity alone or something else?

@curious_cat usually the differences in alleles (at least the coding region of mRNA) are mostly substitutions (which can lead to a change in the activity). Indels are dangerous as they can disrupt the reading frame. Amino acid repeats like in poly-Q diseases arise because of homopolymeric expansion of the CAG triplet. As I said, how poly-Q affects the activity of the affected protein is not fully known. Moreover, different polyQ diseases have diverse kinds of affected proteins ranging from androgen receptor to TATA-binding protein.

Are not all these examples of genetic aberration and not normal functional alleles? Can normal functional alleles have difference in sizes?

@OneFace The disease causing variants are the most obvious, as they're the most studied and have substantial length variation. But even in asymptomatic individuals there's a variation in length for Huntingtin and FMR1. Variations in other, non-disease-associated genes exist too, and I added an example I found from a quick literature search.

One possibility of what you were looking at was a nuclease digestion experiment. A subject's gene sequence could be amplified from their DNA using PCR, giving a band of a certain size when electrophoresed on a gel. The PCR'd product could then be digested with another nuclease that specifically cuts one allelic variant, but not another. For example, check out this rather unrefined image I made:

Lane 1 is the molecular weight ladder. Lane 2 shows the PCR product of our gene of interest, which has two possible alleles - one that can be cut with our nuclease, and one that can't. The rest of the lanes show the result of incubating the PCR product from different individuals with our nuclease. Lane 3 shows a homozygote for one allele, the one that cannot be cut. Lane 4 shows a heterozygote, where the uncut 900 bp band is also seen with the cut 400 and 500 bp fragments. Lane 5 shows a homozygote carrying the cuttable allele on both chromosomes - there is no intact 900 bp band.

This does provide an example of why alleles could run differently on a gel, but fails to answer the underlying question about allele size


text:
Chemoautotrophic eukaryotic cells?
There are heterotrophic prokaryotes, and there are autotrophic prokaryotes. In the autotrophic prokaryotes category, there are photoautotrophic prokaryotes and chemotrophic prokaryotes.
Are there chemotrophic eukaryotes?

There are two ways of classification of Prokaryotes(on the basis of mode of nutrition) that you will generally come across:
Way 1

Way 2

The First classification is very much based on a complete segregation between respiration and photosynthesis. In the first classification, anything that needs another animal to get food is a 'Heterotroph'. (Here, chemotroph and chemoautotroph are the same things)
But Generally the 2nd Classification is preferred, because prokaryotes have some very unique nutritional habits that cannot be explained on the basis of 'Eating/Not Eating'
In a way synthesis is the creation of a carbon compound by use of some energy.
So we need to classify based on energy and carbon source. Here organic carbon source means it is a 'hetero'troph and inorganic means it is an 'auto'troph. Similarly if Light energy is the direct energy required, it is a 'Photo'troph and if a chemical compound is required it is a 'Chemo'troph
By the First Classification, there are no 'Chemotrophic/Chemoautotrophic eukaryotes' meaning no eukaryote can produce food from inorganic material using chemical energy.
But by the 2nd Classification, essentially all eukaryotes that do not photosynthesize, instead use organic compounds as a food source, all animals, fungi etc. are 'Chemoheterotrophs'*However no Eukaryote is a 'Chemoautotroph'


text:
Confluency or confluence, which term is correct to describe the % area covered by cells?
I noticed that both of them are used in many scientific papers. Are these two terms, or can they be used interchangeably?

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

@rg255 Why is this off topic? It seems to be a valid terminology question.

Because it's an English language problem as far as I cam tell

also possibly duplicate http://biology.stackexchange.com/questions/29857/what-does-confluency-mean

Does this answer your question? Origin of term ‘confluency’ in cell culture

Searching Google Scholar for cell confluence returns 239000 hits, while searching for cell confluency returns 75000 hits.
A look at the context in which they are used supports my gut feel, which is that
1:  "confluence" should be used in contexts of "% confluence"
2:  "confluency" should be used in contexts where you describe high or low levels of confluency.

I have conducted a thorough examination of this and find nothing to support your gut feeling, I am afraid. I have documented this in a late answer to an earlier question on this topic.

I have documented the history and current usage of the terms confluence and confluency in cell culture in an answer to another question specifically about the term confluency. As the current question has not been marked a duplicate of that one, and I believe the one answer posted to be incorrect, I am providing a brief answer here and direct the reader to my other answer for full supporting evidence.

Q. Are confluence and confluency two [different] terms, or can they be
used interchangeably?
A. Confluence and confluency, as used in cell culture, have exactly
the same meaning, and usage is a purely a matter of personal preference.

Confluence is a standard English word dating from the fifteenth century, and used as an abstract concept or applied to different phenomena in various fields. Confluency is a term almost exclusively used in relation to cell culture. In this respect, the definition from the short Wikipedia entry on confluency (sic) is pertinent:

In cell culture biology, confluence (sic) refers to the percentage of the
surface of a culture dish that is covered by adherent cells. For
example, 50 percent confluence means roughly half of the surface is
covered, while 100 percent confluence means the surface is completely
covered by the cells, and no more room is left for the cells to grow
as a monolayer.

While there is no guarantee that this Wikipedia entry is correct, it reflects the fact that (1) since the 1960s some authors have used one term and other authors have used the other term to mean the same thing (2) that the same authors have used their preferred term in relation to both the concept itself (without any numerical qualification) and with a percentage qualifier.
I have inspected recent papers in the Journal of Cell Science (referenced in note (9) of my other answer and found that both usages, as above, are still current, as well as mixed usage of both the type prescribed by @MarchHo (confluency, but 50% confluence) and the opposite (confluence, but 50% confluency).
Both terms are accepted by all journals I have looked at, and I have failed to find a pronouncement on the topic by any standards organization or professional body.
Recommendation
Use whatever the people with whom you work use. If you are starting out on your own, make your choice depending on your attitude to the English language or the respect you have for a particular pioneer of cell culture. But, whatever you choose, never tell anyone else that they should do the same.


text:
What is the correlation between hand and neck flexibility?
I am trying to understand this statement in the book, Mudras, Yoga in your Hands by Gertrud Hirschi:

There is a direct relationship between the hands and the neck since the nerve paths run through the vertebral foramina in the arms, hands, and fingers.

Furthermore it is stating that neck flexibility is correlated to hand flexibility.
Where is the vertebral foramina and what is it?

The vertebral foramen
What is it, and what passes through it?

A number of structures pass through the foramen. These are the root of each spinal nerve, dorsal root ganglion, the spinal artery of the segmental artery, communicating veins between the internal and external plexuses, recurrent meningeal (sinu-vertebral) nerves, and transforaminal ligaments.

The nerves in the hand

Starting in the trunk of the body, the nerves of the arm and hand arise from the cervical and thoracic regions of the spinal cord as spinal nerves. These nerves merge to form a network called the brachial plexus before continuing into the arm. Five major nerves extend from the brachial plexus into the arm: the axillary, musculocutaneous, median, radial, and ulnar nerves. Each of these nerves carries information in the form of nerve impulses to and from a particular region of the arm and hand. Some of these impulses are sent from various parts of the brain and spinal cord; some come from sense organs located in the joints, ligaments, and tendons; and some come from nervous tissue in the muscles themselves.

In this paragraph it is specifically stated that impulses received in the hand by receptors, can come from the brain and spinal cord "and some come from nervous tissue in the muscles themselves."
The vertebral foramen is a part of the spinal cord, and forms a vertebral canal, the nerves running through it, and the impulses which are sent could be received by the receptors in the hand. Which could affect flexibility in both neck and extremities.
Sources:

https://www.innerbody.com/anatomy/nervous/arm-hand
http://www.emory.edu/ANATOMY/AnatomyManual/38.jpg
http://medical-dictionary.thefreedictionary.com/vertebral+foramen
https://en.wikipedia.org/wiki/Intervertebral_foramina
https://en.wikipedia.org/wiki/Vertebra
http://www.spinalhub.com.au/what-is-a-spinal-cord-injury/what-happens-to-the-spinal-cord-after-injury/spinal-nerves-up-close


text:
Can some one identify this plant with really sweet smelling flowers?

Could someone help identifying this plant?
The flowers on it have a very sweet smell, similar to the night queen.

Could you add the locale?

Does it have square stems? If it does then it appears to be mint. If doesn't... I don't know :)

@ sanjukta - This was in Singapore

It's most likely a buddleia of some kind, perhaps Buddliea davidii:

You can see the flower is tubular and has four 'petals' at the end. They also have paired leaves, the underside of which is lighter than the top.

The flowers are generally rich in nectar and often strongly honey-scented.

I never thought it smelled like honey, but it does have a very pleasant and strong sweet smell.
It is present on four continents.


text:
Identification of caterpillar in Texas
I found this caterpillar eating my parsley, around Austin, TX.
It looks very monarch-ish, but apparently monarchs don't eat parsley.  Plus it has knobs on its back.
But it also does not look like the Eastern Swallowtail since there is almost no hint of green in its color.
Hoping that this turns into some type of pretty butterfly I am letting it run amok on the parsley for the moment.

Any ideas?

It is the caterpillar of Papilio polyxenes.

The pupae may be green or brown, but not depending on surroundings or the background on which they have pupated. The color of the chrysalis is determined by a local genetic balance that ensures the majority of pupae will blend in.[10] A section of the green pupae will turn a much darker green at the very end of the pupae stage. This color change occurs a few hours to a full day before hatching.[10] Unusually, this butterfly's chrysalis is girdled with a loop, with its feet attached to the silk pad, which helps the butterfly to unfold its very large wings when crawling out.[11]

Here is a photo of black swallowtail caterpillars at different life stages:

Here is a link to a post, which describes all the stages your caterpillar will eventualy go through.


text:
Widest angular of binocular vision

Which out of eagle, rat, duck or owl has the widest angle of binocular vision?

I am pretty sure it's not rat and duck but I am confused between owl and eagle. Can anybody help me figure out which one would have the widest angle of binocular vision?

This sounds like a homework question. Did you do any research yourself on binocular vision?

@Ebbinghaus I did but couldn't really find anything. This is not a homework question I found it in a question paper and wasn't able to find the answer

Take a look at some pictures of eagle and owl and observe their beaks. It will help you in concluding which might have the widest binocular vision angle.


text:
What are all possible vectors for unicellular human parasites?
I got the given question. They want the following pieces of information about protozoological human parasites:

disease - parasite - vector.

There are 10 proteogenic diseases at the Wikipedia. I added the corresponding parasite and the vector next to them:

Malaria - Plasmodium - Apicomplexa
Amoebiasis - Entamoeba histolytica - sarcomastigophora
Giardiasis - Giardia lamblia - no vector
Toxoplasmosis - Toxoplasma gondii - no vector
Cryptosporidiosis - Cryptosporidium - Apicomplexa
Trichomoniasis - Trichomonas vaginalis - no vector
Chagas disease - Trypanosoma cruci - insect
Leismaniasis - Leishmania donovani - sand fly vector
Sleeping sickness - Trypanosoma brucei gambiense - tsetse fly vector
Dysentery - Entamoeba histolytica - sarcomastigophora

I am unsure what I should answer to the question since it is asking "all" possible vectors for unicellular human parasites.
There are many possible diseases, much more than the given ten in my opinion.
It seems also that there are many possible ways of getting the infection for each disease.
I hope that I am wrong in my statements.
It is my first course in Parasitology.
What would you answer to the given question?

This is a good question, because the term "vector" is not used consistently in the literature. This probably is because the context of the discussion is often limited to a subset of parasites. The term is sometimes used to refer to blood-sucking insects. However, animals (including humans) can also be vectors. More generally, anything with mass could be a vector (e.g. biological warfare might use a missile or a blanket as a vector).

Note that if you can answer broader to the question I will accept your answer. It is very difficult for me to accept my own answer so please answer to the question such that your answer is outside of the standard textbooks.

I think the textbook answer is good here, and in line with epidemiological terminology. There are always exceptions, and this topic is outside of my area of expertise. Perhaps you could ask your professor for some more details on the use of the term "vector" - maybe print out this discussion and ask for details that you could use to improve your post.

Based on my course material, I managed to get the following list:

Malaria - Plasmodium falciparum, p. malariae, p. vivax, p. ovale - female anopheline mosquito
Babesiosis - Babesia devergens, babesia microti - tick ixodes ricinus
Balantidiasis - Balantidium coli - waterborne
Coccidiosis & toxoplasmosis - Eimeria species - waterborne
Toxoplasmosis - Toxoplasma gondii - waterborne
Amoebic dysentery - Entamoeba histolytica - waterborne
Periodentitis - Entamoeba gingivalis - oral-oral contact
PAM - Naegleria fowleri - waterborne
GAM - Acanthamoeba species - waterborne
BAE - Balamuthia mandrillaris - waterborne
Trichomoniasis - Trichomonas vaginalis - sexual contact
Trypanosomiasis - Trypanosoma brucei gambiense, trypanosoma brucei rhodesiense - bite of a tsetse fly
Leukopenia - Leishmaniasis specieses - different genera of sandflies: Plebotonus & Lutzomyia

Waterborne means that the parasite is transmitted to the host through contaminated food, water or hands, or by swimming in warm pools or mud pools, for instance.


text:
What is this spider I found in Idaho?

I live in Moscow, Idaho and saw this guy early in the morning last week. It was about quarter sized if I recall. I've never seen one before and was in a hurry so I couldn't get a better picture, sorry.

Looks like female mouse spider. But "Fangs" missing!

This looks like a black trapdoor spider (I'm guessing male by the size of the abdomen), check out the photos on the page I've linked below and see what you think - and this is a pretty good picture, usually the photos friends send me are far more blurry!
http://www.spiderzrule.com/trapdoor1.htm


text:
Validity of measurements of respiration in isolated mitochondria
I've recently read a couple of papers on exercise and mitochondria, in which state 4 and state 3 respiration rates and ROS production are assessed in vitro after exercise has been performed (i.e., rat heart mitochondria are isolated).

Question:
Given that it takes 1 hour for the mitochondria to be removed from the animal and isolated, that additional (saturating) substrate is added before respiration parameters are measured, and that the medium is saturated to the ambient oxygen concentration (much higher than in vivo), are this type of experiment valid to assess mitochondrial function in vivo in active animals? Opinions and/or pointers to resources that clarify how useful these measurements are would be helpful.

What type of cells are these mithocondria being extracted from?

Heart tissue in the case of the above, but also skeletal muscle.


text:
What happens during the fermentation process of the eco-enzyme?
introduction about the eco-enzyme
I have tried to make several ones at home, no matter what I am using, lemon or pineapple peels with brown or white sugar, the final products all show the similar brown colour.
It seems to me that no matter what type of fruit peel or sugar used as the material, would all lead to a similar brown colour.
So I am curious about:
Why the colour of the final product is different from normal homemade fermentative fruit or vegetable?
Are the microbes  involved in fermentation have some difference between the both? Is this because of the difference between enzymes that are produced by bacteria?
I have tried to find the appropriate and availible resource about microorganisms that may take part in the fermenting process of fruit and vegetables, but I am still not sure which one would take part in which step of the eco-enzyme.
(In my observation, some white tiny spots and big speckles began to float on the the surface of the liquid after a week, before opening the container to release gas and make it become aerobic).
What could be the role of fruit peels aside from being the source of microbes,if it will also produce enzymes to influence the chemical reaction?
Is the eco-enzyme really an enzyme?

Why do you keep asking the same question again instead of making the old one better?

I am sorry,perhaps it's because my limited biological knowledge limited the way I ask ,but don't you think the questions this time focus more on the microbes and the enzymes it may produce?

The recipe is using yeast to convert the sugar into alcohol (ethanol). All of the proposed cleaning effect is from the dilute alcohol (and also some vinegar).  The citrus peel provides some aromatic oils. There may be low levels of some particularly hardy enzymes released from the rotting fruit and dying microbes, but it is difficult to imagine that any of those proteins have any effect on removing dirt from clothes, dishes, or surfaces. The solution is also acidic from the fermentation and the dissolved CO2 gas--just like if you used grape pulp and skins you would make a primitive wine with this recipe, and that wine would then turn into vinegar (acetic acid, HOAc).  Mixing some vinegar and alcohol would give you the same cleanser.
The enzyme concentration should be similar to the amount of active enzymes present in homemade beer or wine--would you use either of those for cleaning?


text:
Can the restless leg syndrome may have been caused due to natural selection?
Disclaimer: I don't know how much restless the leg has to be, in order to be considered a syndrome.
RLS runs not only in my family but also several people in the locality. My hypothesis is that RLS is a genetic/epigenetic adaptation to prevent mosquitoes or other insects from sucking blood. I, indeed, live in a malaria zone. I don't know enough biology to device a scientific experiment to prove my hypothesis.
Is there any scientific research done in this field? Someone who is well versed in this field should try it.


text:
Honeybee decision process: new food, new home, new threat
I have heard that honeybees send out scouts, then based on the scout reports more bees go then come back and report and so they are supposed to be efficient decision makers.
Can you give as complete as possible of a description of how honeybee decision making works with regard to:

finding new food/water sources for the hive
deciding where to place a new colony
how they determine if a big enough predator is around to merit a swarm

If you could point to published material that would also be appreciated.
Some links:

http://link.springer.com/article/10.1007%2Fs00265-011-1298-8?LI=true#page-1
http://cis.uws.ac.uk/research/journal/V9/V9N3/bees.pdf
http://www.igi-global.com/article/honey-bee-swarm-cognition/44981

There's also this: http://rstb.royalsocietypublishing.org/content/364/1518/755.

But, realistically, it seems like this, while interesting, is probably too broad of a question and doesn't have a defined answer. In one sense "as complete as possible of a description" is a model; and as in any model building you're going to have to make a lot of subjective choices about which parameters to include, and then a lot of subjective choices to estimate those parameters based on a fairly broad literature.

FWIW the query (bee AND (learn* OR decision OR communicat* OR swarm* OR forag*) AND (model* OR experiment* OR field)) in scopus returns 3000+ hits.

I was looking for something to the effect of the link you provided.  Will try and figure out what SCOPUS is.  http://rstb.royalsocietypublishing.org/content/364/1518/755.full

Scopus is one of the big academic papers repositories – you could use google scholar for similar purposes. When I get time, I'll post links to a few more published papers.


text:
Preferred criteria for new bee colony location
As a human I want a house with a roof, indoor plumbing, bug free, and make my wife happy.  I don't want to drive too far to work, and it has to be well-suited for offspring.
What are the criteria that define a "good spot" for a new location for honey bees.  I'm sure it involves water, shade, access to nectar, and defensibility, but I don't know any of the details.
Has anyone ever made measures of this? Beekeepers? Apiologists?  What are the things bees think are important, and what values of those do they think are "best"?

According to Thomas Seeley, in his book, Honeybee Democracy, he gives the following as important criteria for honeybees when selecting a nest site when a bee colony moves to swarm:

Larger volume (the minimum nesting capacity was found to be around 14 liters with more preference to nests with a capacity of approximately 30 to less than 100 liters)
Relatively small entrance (10 to 30 centimeters squared)
Nest with the entrance located near the floor of a tree cavity
Direction of the nest entrance (south facing for thermoregulation during the winter)
Nest height (preference given to higher nests for colony defense)
Remnants of previous honeycombs (saves work and energy in building the nest structure)

Interestingly enough, bees did not necessarily display a preference for the shape of the entrance, the shape of the nest, the draftiness or dryness of the nest cavity (they are able to plug and waterproof nests).
Flower/nectar/food availability is not necessarily a direct factor as this changes quite frequently throughout the seasons and honeybees are not able to leave their honey stores (which are necessary to sustain the colony throughout the winter) or take them with them every time the colony has trouble finding food. Honeybees have a complex and efficient system for optimized location and sharing of food sources, therefore distance is not as large a factor.

I assume you're talking about keeping honeybees apis mellifera , not other species.
Beekeepers often move there hives around to follow nectar availability, so I assume nectar availabilty is considered the most important factor.
In my country the first to flower is willow salix. After that they move to cherry&plum tree plantations and after that to appel&pear.


text:
What type of insect is this?
I'm naturally thinking this is a bee, but I cannot find it anywhere in any insect identifiers. I caught this picture on top of my doorway, it's about 1 1/2 inches in length, and its torso seems to be coated in a layer of hair, and the rest of its body is narrow. The thick layer of hair may or may not be accurate, I didn't want to get too close to it, but that's how it appeared at least.

What is this?
PS - Found in Kentucky, and I'm not sure why one pic shows wings and the other one doesn't...

Well I can suggest why the wings are not seen in two of the pictures. From the shadows it is obvious you have not used the flash. Under natural low light the shutter remains open for a longer time and any movement of the wings will blur it. In the third picture you must have got when the wings were not moving.

Well I was using a camera phone

It's a red-footed robber fly, check out those lateral stripes and the red/yellow leg segments

From the general body plan, it looks like it's probably a robber fly. Here's a page of specifically Kentucky robber flies – it's possible yours could be a Bearded Robber Fly.

That looks about right

It is most certainly a Robber Fly. I would agree with Oreotrephes that it is a Bearded. I can't seem to find anything closer.

My first idea as well, but the picture is probably to unclear for a certain species determination.

Yes, I would say that is a bearded robber fly. Robber flies are similar to dragonflies in that they catch prey by catching it in midair. They will attack mostly bees, wasps, and hornets, and I have seen many catching bumblebees in the wild. I have even seen some sit near a yellow jacket nest and catch a hornet when it comes out. They suck out the juices of their prey with a proboscis using methods similar to spiders. They will also bite when handled, as I have found out through experience.

It is commonly called as "Robber fly" or "assassin fly". Scientifically it is "Asilidae" of the order "Diptera" and it is a fast attacking predator mostly preying on grasshopper nymphs and damsel flies. It is strongly built for kill.
http://www.robberflies.info/keyger/htmle/didpic.html

Can you provide some references for your answer? Please read the help for this site, in particular here where you can know how to write a good answer.

http://en.wikipedia.org/wiki/Asilidae

Also posting a separate image of your ID is important to allow other usres assess your answer


text:
Would boiling water kill microorganisms in clothing that had feces spilled on it?
Lets say there is a piece of clothing that had a small amount of human feces that spilled on it.
Would placing that clothing in boiling water destroy the microorganisms on that clothing?

I'm voting to close this question as off-topic because it is about health or domestic science rather than biology.

It has nothing to do with health or domestic science.  It is about biological concepts and biological mechanisms.

The question you quote is just a question from one person expressing his opinion in the same way as I was. His opinion is not SE policy, and mine is not unless four other list members with sufficient privilege vote to close your question.  2. I do not think disinfecting clothing is to do with either biological concepts or mechanisms. 3. If your comments are addressed to a particular poster you should include an @ followed by his name. That way he will be notified of your posting.

Whether boiling water is hot enough to kill skatole, stercobilin, haem, bilirubin and biliverdin are biological concepts.

...kill skatole, stercobilin, haem, bilirubin and biliverdin... -- these are names of chemicals, but your question asks about microorganisms. Are you interested in the denaturing / removal of chemicals or the killing of microbes?

Using boiling water alone will not destroy all the toxic compounds found within faeces. One example is skatole, this is found in faeces and is partially responsible for the foul smell faeces gives off. By laundry I assume you mean laundry detergent? If so, it would depend on the detergent being used.
I hope this answered your question :)


text:
Where are newly discovered medicines tested
When a medicine is prepared by a biologist,then where does he first test on? And how does he know that this is the exact combination for a disease to get cured? Does he test that medicine on a human or specific sample of blood? I'm an engineering student but still I'm curious to know.

This is a very broad question, so I won't attempt to answer it fully. Instead, I'd recommend starting out by reading the Drug Development and Drug Discovery articles on Wikipedia, and if you have more specific questions after that then feel free to ask them here.
Basically, new drugs (either small-molecule "chemicals" or large-molecule "biologicals") are discovered in myriad ways, from pure accidents (see Penicillin) to specifically-targeted research. Once a lead compound is identified, it is put through a series of biochemical assays to determine, for example, if it inhibits certain enzymes of interest. From there, it moves into testing by cell-based assays using both normal cells and disease-specific models. All the while, investigators are looking for high specific activity (potency), low toxicity, and minimal off-target effects.
If a compound or group of them looks promising in these in vitro assays, experiments then move into animal models. The goals are similar here - high activity, low toxicity, and few (if any) side effects. The experiments get progressively more complex, with different endpoints depending on the exact aspect being studied.
It is only after extensive animal testing that a compound will be tested in humans. There are different phases of testing, each with different criteria, dosing patterns, number of patients, and reporting rules. The link I just gave explains each phase briefly.

Hopefully this is enough to get you started. Like I said earlier, if you have more specific questions after reading through all the references, please let us know.

Just to put all of this in perspective: this whole process (when properly done) can take around 15-20 years and a few billion euros.


text:
What are the methods for infering genetic interactions?
Is there a classification of methods for inferring genetic interactions? I mean some work published, utilizes genetical genomics data.  Is this possible with expression data alone? And how about perturbation screens? I guess they all need information about mutants/genetic variations?

The questions is vague and difficult to answer because there "genetic interactions" is a catch-all bag for anything that isn't a monogenic trait - which is to say, most of them.

BioGRID is an interaction database, and they catalogue interactions by (among other things) the class of experiment that discovered them. See http://wiki.thebiogrid.org/doku.php/experimental_systems#genetic_interactions
Other than that, you should look at recent reviews and publications, but you will easily get lost unless you figure out some important particulars, like:

What species? Yeast, worm, human, cell line?
What sort of interaction? Synthetic lethality? Complicated, fancy epistasis?
How much? Genome-wide? 2-3 genes?


text:
Does a piezoelectric organic substance exist?
that contracts rapidly, in 10 seconds or less, by .5mm or more, when bombarded by electrons as from a cathode ray tube? or expands? could either be living tissue or dead organic matter.  thanks!

I don't know if it would contract by the amount that you are after, but bone (which has both organic and inorganic components) is piezoelectric.
For an overview, see http://silver.neep.wisc.edu/~lakes/BoneElectr.html.

They suggest that two different mechanisms are responsible for these effects: classical piezoelectricity due to the molecular asymmetry of collagen in dry bone, and fluid flow effects, possibly streaming potentials in wet bone.

I think your question is a bit specific, but piezoelectric organic substances do exist. There was a paper in nature that researchers at Berkeley published.
Please see the following journal article:
http://www.nature.com/nnano/journal/v7/n6/full/nnano.2012.69.html#affil-auth
Also see the following public article:
http://www.extremetech.com/extreme/129389-berkeley-scientists-turn-harmless-virus-into-piezoelectric-generator


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What is the significance of and biological mechanisms demonstrated in lac operon?
I would appreciate it someone could explain clearly how the genes in the lac operon of E coli are activated to allow the bacteria to metabolize lactose?
The part that I really don't understand is the activation of the lac operon.  A good answer would make clear to me how the introduction or removal of lactose from the envirnment activates and deactivates the different genes there.
Also, what are the specific functions of each of the genes (lacA, lacI, lacY, lacZ).
I am in AP Biology and I will not see the light of day again if I do poorly on this test. Please help!

You'll have to be more specific about which aspects of the lac operon you don't understand, currently this question is far too broad.

There are many good youtube animations and videos which might help you !

just trying to help - I made some edits to illustrate what they want.  Feel free to roll them back if you don't like them.

The lac operon in E coli is a set of four genes which work together to allow the bacterium to make use of lactose for energy. An Operon is a set of genes which are co-transcribed on a single mRNA, controlled from a common promoter.  While operons are nearly always found in bacteria, eukaryotes (and viruses that infect eukaryotes) do have some sets of genes organized into operons.
lacZ and lacY is the business end of the lac operon. They are the only 2 genes necessary for lactose usage in the cell.
lacZ codes for beta-galactosidase, an enzyme that cleaves the lactose disaccharide into D-galactose and D-glucose.  Most of know that glucose is an important source or energy via the glycolysis pathway, which is highly connected energy usage in the cell.  Galactose is readily converted by an enzyme (galactose mutarotase) into glucose, making lactose an efficient source of energy.

lacY codes for a protein found in the cell membrane called lactose permease which pumps lactose into the cell from the outside using the proton gradient inside the cell for its motive force.
The lacA gene codes for an enzyme which transfers an acetyl group to galactose, which may prevent the buildup of galactose in the cell.
The way the operon works is more important than what it does.  the lac operon was one of the first examples of transcription regulation every studied.  lacI is not in the lac operon, but it is the single gene which controls whether the operon is copied to RNA from the chromosome.  lacI is translated to the lac repressor protein (LacI), which binds to one of three sites in front of the lac operon.
lacI is a repressor gene - when it is active, it prevents the lac operon from being transcribed into RNA.  LacI is a tetramer - four copies of the protein form a complex.  LacI binds to allolactose, a derivative of lactose, when it is present in sufficient quantities, which then causes it to release itself from the chromosomal DNA, allowing transcription to occur and the lac genes may be expressed.


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Is Zymase, A Complex of Enzymes? Which ones?

Some websites state that the enzyme zymase (which I understand to be a complex of several enzymes) is responsible for catalyzing glycolysis in order to produce pyruvate.
On the other hand, some other websites state that zymase is responsible for catalyzing the conversion of pyruvate to acetaldehyde, and acetaldehyde to ethanol and carbon dioxide.

Which one of the above is correct? And, what are the names of the enzymes that are collectively called zymase.
I thank you for your time and consideration. Good day!

This is all correct it seems, but maybe the term is more of historical interest rather than current science.
Zymase is a term which is no longer in use in the scientific literature.  It seems to have disappeared in the 1950s.   The latest reference I can see is 1970s.
The reason seems to be that Zymase was purifiable from yeast with 19th century techniques.  The term was coined in 1897.  This is probably because in brewers yeast the Zymase components are either in a protein complex or contained within a compartment in the cell that could be separated from the rest of the organism.  Here's an early reference - german isn't so great.
The Zymase activity was shown to vary from one strain of yeast to another, which makes the discovery seem more a manifestation of the physiology of that one strain of yeast.
Later work showed that Zymase activity was organizable into a more universal set of genes which are conserved in all living things and called the 'citric acid cycle' or the Krebs Cycle. Krebs performed his work without reference to Zymase, where biochemicals were added to a culture and their transformation tracked. So, Zymase seems more like a historical footnote...
Wikipedias' entry sounds as if the extraction was not very pure - its called a 'press juice' so I think it would be difficult to describe exactly which specific enzymes were in Zymase.  I'd naively assume that nearly all the citric acid cycle enzymes would be involved in Zymase activity, where observed.
Many of the enzymes in the citric acid cycle form large complexes with themselves and other of the enzymes, which might be responsible for the original discovery of Zymase.

The linked german paper is a reproduction from 1935, so I don't think it is evidence that the term is still used

good point - fixed.


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What is the datatype of dna sample?
What is the type of data you get when analyzing dna of a person? If you want to store them in a database, what type of field you will need (text,number,hex)? And what should be it's length?

Assuming that you are looking at data used to describe the differences for a new individual, as opposed to a human reference genome build:
A fastq file is the typical format of data from a sequencer.
It would require a text field of some sort as they can be quite large, even for single reads.  If you had a specific sequencer in mind with very short read you might use a fixed length field for the data column, but its probably not worth it.
After the data is processed, then the data is currently usually exchanged in the form of Variant Call Format files (a vcf file) which only documents differences versus a reference genome build.  This fits nicely into an SQL table with relatively small columns.

It will be a simple string of text. The length, however, is completely arbitrary and will depend on the source of your sequence data. Anything from 1 to several billion can be a valid sequence length.
We could help more if you explained where the data is coming from.

Realistically, you aren't going to store the genome as one long string of text.  Depending on how you do the sequencing, you probably won't be able to resolve repetitive regions anyway.
What is much more realistic is you will store all the differences you are confident of between the sample and a reference sequence.
If you use some kind of genotyping chip, you'd store the genotypes at each locus.


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Which of this 2 affirmations is more close to the explanation of evolution?
I am almost secure that this affirmation aren't exactly true but I want to know which of these statements is more near to a description of how evolution works:

The evolution has an exactly target and always progress to it, each generation the childs are more close to make complete a certain task, that is beacuse evolution is like "directional".
For example: The task is be 10cm taller. Each generation the race become 1mm taller up to complete the task.
The evoultion is random but the specie (or natual selection) try to reach a target, each generation has random traits but only benefical traits tends to "survive" and get offpring.
For example: In order to survive the task is be 10cm taller. Some childs are half cm taller and other childs are half cm smaller, the last ones die naturally and only the taller ones survive enough to get offspring.

This seems like it's some sort of homework assignment, though I am afraid even the better of the two is hardly any better.

One is better but is still awfully unclear, poorly phrased and misleading. I don't feel that if you were to know which one is better, it would not help you much to get basic understanding of evolutionary processes. The best for you is to start with a short and easy intro course such as Understanding Evolution by UC Berkeley for example.

@BryanKrause given how bad the phrasing is, I think we can be clear this not a homework and could answer which one is better, right? So, here we go: The second one is slightly better!

@BryanKrause, that isn't a homework! We don't have biology in school, it's only a curiosity of me.

@Remi.b, sorry for my grammar, english isn't my main language. It's a curiosity that I have, not a homework.

@EnderLook No worries. I am an ESL too and it is not uncommon that other users correct my grammar.

@Remi.b You'd be surprised at the quality of education in some places, especially on evolution...

@BryanKrause Yeah, I agree. For being part of the Evoke community (committee acting on improving education in evolution at all levels in Europe), I also came to realize how poor can be the quality of education in evolution even in countries that normally have good science education (esp. in high school). We have actually already witness a number of very bad homework questions on this site.

@Remi.b This is not a homework (In 5º year of high school we don't have biology)... and I don't live in Europe so I don't think that Evoke would work in my country. Sorry for my poor knowledge about evolution, I was only designing a creature for a ficitonal world whne suddenly I get the curiosity of how that perfect creature (it's to much perfect, too much) could have evolved and then I write the question... sorry.

@EnderLook Don't worry, very few know about Evoke and it really is a side discussion to the post. Bryan and I kind have a side chit chat here (which we probably should not have)!

The second is marginally better because it mentions randomness and emphasizes differential survivorship, but the parts about "trying to reach a target" and specifying a particular "task" are misleading at best. I would rewrite the statement as follows (I have edited for grammar, spelling and style as well, but emphasize more substantive deviations with strikeout for omitted parts and boldface for added parts). The substantive edits change the meaning of the statement significantly: most evolutionary biologists would be very uncomfortable with the second statement as written above (setting aside any grammatical issues).

Evolution is has a random component but the species (or natural selection) tries to reach a target, may result in directional change: each generation has some random variation in traits but only individuals with beneficial traits tends to  are more likely to survive and produce offspring. For example, In order to survive the task is be 10cm taller. taller individuals survive better than smaller ones.  Some offspring are a half cm taller and other children are a half cm smaller; the latter die naturally and only the taller ones survive long enough to produce offspring.

I would probably say "offspring" rather than "children" in a technical context.
Note also that this emphasizes evolution by natural selection; broadly speaking, there are many non-adaptive processes (vicariance, drift ...) that also lead to evolution (change in gene frequencies between generations).

I would remove Evolution is random or maybe jsut edit it to Evolution is partially stochastic or even better Evolution is not a purely/uniquely deterministic process or even Evolution is the results of a number of processes, some of them being deterministic, some being stochastic. Good answer otherwise +1.

Thanks for the answer. Sorry my poor grammar, english isn't my main language.

@EnderLook I just want to clarify for you especially as ESL/ELL, that this answer is correcting more than just grammar.

Don't worry about the grammar, by the way. I modified it because I'm a perfectionist, but there's nothing wrong with trying to express your ideas (my second-best language is much worse than your English).

@BryanKrause, I know, I am no so stupid ;).

@BenBolker, I know, I am not worried about that, I also do the same to other people (but in my main language), about the second-best language... I don't know more language that english and spanish :(.


text:
How do GPCRs transmit a signal across the plasma membrane?
How do G-coupled protein receptors (GPCR) transmit signals through the plasma membrane?
Links containing information about this and pictures will be very helpful.

The G-coupled protein receptors (GPCR) transmit signals from outside of the cell into the cell and activate downstream signalling pathways. These change for example the expression of certain genes.
The whole process is a coorperation between the receptor, a G-protein, GTP as a co-factor and the ligand of the receptor (which starts the whole process). An extensive description (including much more images) is available in the Wikipedia, but in short, it looks like the images below (from the Wikipedia article on GPCR):

To answer how this signal is tranferred from the outside to the inside look at the first image: Upon ligand binding the conformation of the receptor changes its conformation and brings some of it transmembrane helices together so the G$\alpha$ subunit can bind here and activate downstream signalling.

The whole process happens in a few steps:

In the resting state the receptor has a trimeric G-protein (consisting of the subunits $\alpha, \beta$ and $\gamma$ bound on its cytosolic site. The G-protein also has a GDP molecule bound to it $\alpha$ subunit.
Upon binding of the ligand, the receptor changes its conformation, and G$\alpha$ exchanges the GD against GTP, which activates the complex.
The G-protein dissociates into the active G$\alpha$ the G$\beta\gamma$ subunits, which signal to downstream signal transduction pathways like the MAP-Kinase pathway.
Binding of RGS (regulator of G-protein signalling) to the g$\alpha$ subunit activates the intrinsic GTPase function of the subunit and hydrolyses GTP into GDP and P. The GDP stays bound to the G$\alpha$ subunit, which changes its conformation and forms the G-protein trimer at the receptor. At the receptor itself this induces also a change in conformation which makes the ligand dissociate from the receptor.

At the end of the fourth step the receptor has returned into its inactive form and stays there until the next ligand binding.

Thanks for your help.but intracellular signal transduction is well known property of gpcr i know the mechanism of that.i asked how gpcr transmit signal through plasma membrane

@N00B I added some information. But the whole process (especially the involvement of G-alpha) is connected and can not be seen seperated.


text:
Won't natural selection miss the overall minimum of a function?
Suppose we have a population of about 1000 with an environment that does not change a lot (e.g. the atmosphere is more or less the same) and we leave this population to evolve. From what I understand some genes will be lost because they won't be suited enough to continue in the next generation. Also the generations can only reproduce within their generation (e.g. a male can only have reproduce with people from his generation).
My question is: won't some genes, combined with others have a better chance to make the individual "better" but they for example make it less fit right now. Or will the mutation of the genes actually promise that eventually we will hit that minimum of the function.
I want to point out that I'm a computer scientist and my biology is awful. I'm looking at this from evolutionary algorithms point of view in particular genetic algorithms.

Can you clarify what you are asking?  That second paragraph is very confusing.

As in evolutionary algorithms (you might know from computer science), real evolution is random. It might hit a local minimum, but miss the global one. Different to evolutionary algorithms, evolution can even make things worse for a while, so there is a chance to have a "bad" mutation "surviving" long enough to be paired with another mutation that actually makes it "good". But it is random.

Indeed your second paragraph is confusing. What function are you talking about. It seems that in you example, two individuals with the same genotype in the exact same environment have different fitness. It is theoretically not possible. Does your question has to do with genetic interactions [http://en.wikipedia.org/wiki/Epistasis] or gene-environment interactions [http://en.wikipedia.org/wiki/Gene–environment_interaction]. What does your question has to do with game theory? Are you talking about newly arising mutations or only about alleles (gene variants)?

Your second paragraph starts with "My question is..." but does not actually contain a question. What are you asking? There is a well known mutation that  makes individuals susceptible to sickle-cell anaemia but the same mutation also protects from malaria. Is that the kind of thing you're thinking about?

It sounds like you're asking about local minima that is, "dips" you can get stuck in though there might be a "valley" next to you?

If this is what you're asking about, I think is referred it as a "stable state". In ecology, we think about "alternative stable states" all the time, and certainly some might be "lower" than others on whatever metric you're measuring. I think the real question from a modeling perspective is is the population stochasticity/"jiggle" large enough to get over small humps?

You're absolutely right. Evolution is path-dependent. It can't progress toward features that would ultimately enhance fitness unless each step enhances fitness by itself.

@octern This depends on population size. Founder effects or stochasticity in small populations can cause traits to go against fitness gradients, which could potentially bridge local fitness valleys.

Perhaps it would have been more accurate for me to say that selection can't progress in that way. You're right that the overall process of evolution includes random events that prevent it from being a pure fitness maximization function.

very tempted to downvote this, please elaborate on what you mean by overall minimum

What I think the question is "Why wouldn't an organism be more efficient from selection than the environment demands?"  Please let me know if I'm hitting the mark here.
A scenario suggested by the question is this: If there is selection pressure on say an animal to resist a disease, and then it evolves two resistance systems to the disease.  This could be an immune response and a taste for a certain plant containing compounds with remedial properties.  If either system is adequate to resist the disease, hasn't selection gone above and beyond what is needed?
If so, the answer is either not recently, or all the time.
First, for 'not really' you have to consider the importance of competition.  Reading about the Red Queen's Hypothesis is helpful here.. First there is a natural random mutation rate, which can cause one of the system to become less effective.  Or if the disease is also changing to increase its efficiency, then either one or both of the defense mechanisms in this case would fail from time to time.  Then having two systems would not be too much. There is a clear benefit to having redundant systems of resistance here. For both these broad categories of reasons, you have much redundancy and interdependence among the genes which create traits in living things (phenotypes).  Because of the background mutation rate, traits which are not needed disappear relatively quickly; because of competition, those which convey an advantage, even if a small one, have a strong likelihood to stay in the gene pool.
now: "all the time" There are cases where traits are exhibited that are not efficient though. Evolution works over generations, typically selection influences traits on the order of 10s of generations and the population can show traits which are not helpful if the environment or the competition has changed drastically.
An example of this is the current obesity epidemic in the developing world. The sudden availability of cheap food has caused those people who have access to become obese.  This is because they have a heavily reinforced trait to save up fat because humans experience famines regularly.  Its going to take a long time before efficient energy storage in human beings is lost.  In the meantime, people are not living to reproducing age at the same level of fitness they might have.
I want to add a note on genetic algorithms.  The difference between genetic algorithms to achieve the same efficiencies as biological systems are worth thinking about:

As far as failing to find a global minimum, natural selection usually has many more samples.  A typical selection experiment with flies or worms often have thousands or tens of thousands of individuals screened.  GA models of reasonable complexity have usually a few score at most - am I right?  A bacterial or yeast experiment can have 10^9 individuals.

The genetic system of the chromosome itself is tremendously complex.  We can't even model itself and so the product of millions of generations of selection already will has a heretofore unmodelable response to selection.
The typical selection environment is equally undefinable, so a survey of living things in a complex environment has unpredictable effects.  While most of us think as laboratory experiments as being less complex, its not completely true.  I was at a talk recently that mentioned how E coli K12 seems to have diverged in various laboratory environments despite the fact that its mostly been in frozen stocks since being isolated in the mid 20th century.

Re: Red Queen's, van Valen's original paper has perhaps the best acknowledgement ever: "I thank the National Science Foundation for regularly rejecting my (honest) grant applications for work on real organisms...thus forcing me into theoretical work."

@Oreotrephes That's amazing.

@Oreotrephes Van Valen's paper is wonderful in all its weirdness, and provides useful perspectives on scholarly communication.

I'd not read this either - thanks @Oreotrephes!

Im going to take a stab at this. I think he is saying that sometimes there will be mutations that will occur in a population that are beneficial, but only in certain environments. But he is asking, wont these mutations be eliminated often, since they may not be in an environment where their advantage is obvious?
First, there is something incorrect in your original post. You said "From what I understand some genes will be lost because they won't be suited enough to continue in the next generation". It is kind of unusual for a whole gene to be lost. Especially from a whole population! I think what you mean is 'allele'. And yes some alleles will be lost. But fitness is a gradient. Just because a mutation does not have an obvious advantage does not mean it will be lost. Most mutations are not really noticeable. In a recent post here, I think I quoted a website that says there are 70 or so de novo mutations every generation in humans. This means that both you and I have 70 new mutations that our parents did not. But we are both functioning just fine (I hope!).
And some of these mutations may be beneficial in certain environments, but dont do anything in others. Lets say that one of my de novo mutations was to make me sweat less. Not really noticeable, right? And it really wont give me fitness advantage or disadvantage, so natural selection wont really act on it. It's frequency should remain at about a constant level in the population . But now lets say something happens to the world climate and there is a drought that lasts for centuries over N. America. My mutation would now give me a fitness advantage since my body would lose less water.
So, to answer what I think your question was, natural selection will not always act on every mutation. It has to clearly give a fitness disadvantage to select against it, or an advantage to select for it. So if it gives no immediate advantage, it may not spread through the gene pool very quickly, if at all, but it will still be there. So when it is in an environment where it is advantageous, it will still be around, and then it will begin to spread through the population.