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Human Papillomavirus E7 (HR HPV16)
So there's a protein that binds to E7 viral protein, I want to remove a sub domain of the protein to see which exact domain the E7 binds to.
What is the procedure for this?
Edit: I believe the virus is HR HPV16. I need to know a method/procedure that can allow me to delete/mutate the NLS, CXXC ,BAH1 and BAH2 domains in the enzyme DNMT1

Welcome to SE Biology. Unfortunately your question is unclear as it stands. What virus are you talking about? When you say you want to remove the subdomain are you talking about work with the gene or the protein? And what do you mean by "What is the procedure?" How much work have you already done? What research have you done? We need to have that sort of information if we are to try and help you.

Thank you David :D I believe it is the HPV E7. And I am talking about work with the protein. I'm actually a bit confused myself. I will update as soon as I get more information

Oh and David, I sent you an email regarding further information on this. I hope you don't mind.

Please do not send me personal emails. This is a question and and answer site. When someone makes their first post, it is flagged to older members of the list so that they can make suggestions, if necessary, for improving it. That is what I did to prevent your question being rejected and to incease the chances of your getting an answer. I personally shall not be answering as this is not my field of expertise.

Ahh I see. I apologize


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Suggestion about head transplant
The success of the head transplant surgery depends on the acceptance of the immune cells of the body on which the head is going to be inserted. Can stem cells from thymus gland and bone marrow of the head donor be transplanted into the body on which the head is going to joined, then those stem cells will produce lymphocytes which will accept the transplanted head. Can this be a way to increase the probability of success of the head transplant operation?

Transplanting bone marrow is already done as a therapy for leukemia and is a transplantation with the risk of rejection itself. It is painful, risky and complicated. A person undergoing this would likely for a long time not be healthy enough to undergo yet another transplant.

I think that immune rejection is not the only major problem in head transplantation.
We are quite skilled at suturing vasculature, but it's not fully solved yet how can you make new and proper connections in the spine?
Concerning your questions, if you just took these naive lymphocytes, they would probably get destroyed by the acceptor's immune system pretty soon. If this wasn't the case, the approach would already probably be in use for other transplantations too.
What you possibly could do is a bone marrow transplantation, where you would replace the bone marrow of the acceptor with that one of a donor. However this would cause the opposite problem, the donor cells attacking the acceptors body.
For now, lifetime immunosuppresion is the only working way to go.
To get a better idea about how exactly the mechanism of rejection works and the prospective future therapies, see for example: http://emedicine.medscape.com/article/432209-overview#a8

"What you possibly could do is a bone marrow transplantation, where you would replace the bone marrow of the acceptor with that one of a donor. However this would cause the opposite problem, the donor cells attacking the acceptors body" : What do you think of this https://biology.stackexchange.com/questions/79881/could-bone-marrow-transplants-be-used-to-prevent-tissue-rejection-of-trans-speci as a fix for that, introduce both patient & body donors cells to the pig fetus then transplant it's bone marrow?

source: Stack Exchange

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

sort: votes


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Orange Fungi on Oak tree
The fungus in my profile pic is bright orange in a ball growing out of the cut off branches scar, also in a necklace.  There are egg shell white broken balls instead of the orange balls-suggesting the orange ball explodes and the seed depart leaving the white shell bottom.

The picture is missing, please add it for clarity.

@Chris look at her profile pic :-)

Too small! Can't see detail! :(

http://leslieland.com/2009/09/hunting-laetiporus-sulphureus-the-sulfur-shelf-or-chicken-mushroom/  I think this is the answer.  I have great pictures, but don't know how to add them.

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


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What is this green micro-organism found living in water?
I study biology in France and experiment on water filtration with plants. I found that some chlorophyll-containing micro-organisms (about 10 micrometers in length) were raised in my basin.

I can't decide if this is a eukaryote (it looks like there are cellular compartments) or a prokaryote (it's very small!). I thought it could also be a cyanobacterium, that combines features of both prokaryotes and eukaryotes. Any ideas what this is?

I can't decide if it's a eukaryote or a prokaryote.

Well, that's certainly an eukaryote. We can clearly see the nuclei in the cells of your fist picture, as well as in the cells of your second one (not so clearly, though):

In the image above, the arrow starts right on one of the nucleus of that group of (apparently) three cells.
Besides that, despite some cyanobacteria being very long, 10µm is a lot for a prokaryote. The mean size of cyanobacteria is way less than that.
By the way, this:

... a prokaryote or a cyanobacteria (that can combine both characteristics)

Doesn't make much sense, because cyanobacteria are prokaryotes. More precisely, they are Eubacteria prokaryotes.
Finally, what eukaryoyte is this? I can't tell. It's most probably a kind of Chlorophyta, but I'm not able to go to the Class level. If you're interested in identifying it, you can try a taxonomic key. This one is for British freshwater algal flora, I don't know how different French algae are from the british ones: The Freshwater Algal Flora of the British Isles: An Identification Guide to Freshwater and Terrestrial Algae.
If I'd guess (and this is a wild guess), I'd say that this is a Chlorellales, as the famous Chlorella:

Also, have in mind that saying "that's an alga" doesn't help as well: worse than paraphyletic, algae  is a polyphyletic group and, in biology, polyphyletic groups mean almost nothing.

Have you considered that it might be algae? (I think it is.)

There are many kinds of algae. I couldn't tell you which one yours is.
Algae Under Microscope


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Need / consumption of magnesium
Does doing sports makes a human require more magnesium and – if any – how strong is this effect?
Do athletes take magnesium supplements (e.g. pills of magnesium carbonate) because they build muscles and therefore need more of it as their muscle masses increase, or is magnesium consumed by muscle activity (e.g. by causing a chemical reaction which the human body can't undo so it has to excrete the reaction product and get new magnesium from food)?

@Xaqron You should post that as an answer.

Strenuous exercise apparently increases urinary and sweat losses that may increase magnesium requirements by 10-20% according to this paper.

Is magnesium stored in muscles / do you need more when gaining muscles?

@UTF-8: You are correct. Please check here for more info.

I don't see how the linked page says anything about where magnesium is stored or whether you need more of it if your muscle mass increases.

@UTF-8: Your assumption is true and the like contains a table for magnesium needs in different ages/gender. According to table 0.5 gr/day is maximum someone may need.

Sweat and kidneys remove magnesium.  Some foods and medicines retain potassium. Exercise will move salts indiscriminately.  Kidneys try to keep a balance.


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Can bacteria be considered carnivores?
Ok carnivores are "animals that eat other animals," so what are bacteria that eat animals? Or are they just not important

I think it's more that bacteria are a special case. As they don't directly consume anything, taking the so-called "flesh eating bacteria that cause necrotizing faciitis as a good example: they simple release compounds or toxins that break down the surrounding matrix or tissues and absorb the products. In that sense you could call them saprophytes, saprovores or saprophages: organisms that consume decaying organic matter.

Welcome to Biology.SE! "carnivores are animals that eat other animals" well, its a bit different. A carnivore is an organism that derives its energy and nutrient requirements from a diet consisting mainly or exclusively of animal tissue, whether through predation or scavenging. Bacteria ain't that choosy, are they?

I'm voting to close this question as off-topic because it is not about biology. It is an attempt to provoke a pointless discussion of semantics.

@David I disagree; understanding how technical words are defined in a scientific field and why those definitions were chosen is about as pointful as semantic discussions can get. It looks to me like there's the potential for good and informative answers there is what i'm saying. Unless "attempt to provoke a pointless discussion" is an informed statement about the OP's intentions (i.e. they're an outright troll) of course.

@RozennKeribin — I call them as I see them. You are entitled to your opinion, but I do recommend that you reread the tour to this site and especially https://biology.stackexchange.com/help/dont-ask, and then consider whether questions are or are not in the spirit of and useful to this site.


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Are bacterial RNA polymerases distributed evenly throughout the cell or localized?
Bacterial cells aren't internally compartmentalized with membranes (like eukaryotes). This naturally leads to an image of a homogeneous interior, but bacterial cytoplasm isn't homogeneous. Case in point, the DNA is localized in the nucleoid. If the cell goes through the trouble of putting all its DNA in one spot, having RNA polymerases everywhere would be pretty wasteful (even counterproductive). So, is the more intuitive image of bacteria, with RNAPols everywhere, right? Or are they localized? If so, how?
If species matters, lets primarily talk E. coli.

In E. coli most RNA polymerase molecules are bound to DNA, and those that aren't are within easy reach of the DNA.
According to Larry Moran

A typical E. coli cell contains about 5000 molecules of RNA polymerase. When the cells are growing rapidly, 2500 molecules will be bound to genes in transcription complexes. Another 1250 will be in initiation complexes of various sorts and most of the remaining RNA polymerase molecules (1200) will be bound to DNA non-specifically. Only a small number (~50) will be free in the cytoplasm.

The numbers that he quotes for number of molecules of polymerase and proportion that are engaged in transcription are in reasonable agreement with values available at Bionumbers. So it seems that most RNA polymerase molecules will be located in the nucleoid; any molecules that are free in the cytoplasm are within easy reach of finding a DNA binding site since a typical protein can diffuse across an entire E. coli cell in 10 ms. (Bionumbers)


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Can qPCR primer with several mismatch works?
I am designing primers for qPCR from conserved regions of a few different fish species.This is because gene sequence for my fish species are yet unavailable in NCBI database.
Is it OK (can the primer anneal to the target sequence) if the primers have several mismatch at the interior and towards it 5’ end? At the 3’ end, I can only design primer with maximum 5 conserved bases.
Thank you.

qPCR will not work reliably with so poorly matched primers, so either create multiple primer sets with higher specificity or create multiple primersets amplifying subsets of the target... this will create multiple better fitting fragments, that will act as optimised primers in later rounds of the qPCR experiment... keep in mind that the latter option will produce quite a lot of background noise.

QPCR is extremely sensitive, so I would not do this. Instead I would get those primers you mention in your question and instead sequence using them instead of doing qpcr with them. Then I would make new primers specific for the region you want to do qpcr on based on the sequence.The advantage of this is that you would now know the sequence and so you would have better primers for qpcr.


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What is the difference between cytosol and cytoplasm?
I've generally seen cytosol defined as the solution inside cells minus  the organelles, cytoskeleton, etc and cytoplasm as the cytosol plus the organelles, cytoskeleton, etc. This naturally leads to the impression that cytosol is the cytoplasm minus all the solids. The problem here is that there are all sorts of other large molecules in the cells which could be thought of as solid. Are they also part of the cytosol or are they suspended in it? (I.e. are they part of the cytosol or are they non-cytosol components of the cytoplasm?)
Basically, I'm asking if the precise definition of cytosol is just anything in the cell that's not behind an endomembrane (save the exoskeleton) or if the dividing line is something else.
Subquestion: things can get even more terminologically confused because the cytosol is sometimes called the matrix. What the heck is the preferred terminology with this stuff?

'The problem here is that there are all sorts of other large molecules in the cells which could be thought of as solid.' Can you give some examples so that we understand how you are using the term 'solid'?

IMO, the definitive answer to this question is given in a paper by J. S Clegg.  He traced the origin of the term cytosol to a book chapter by H. A. Lardy, and confirmed by email that Lardy had indeed coined the term. Their definition of cytosol is as follows:

... that portion of the cell which is found in the supernatant fraction after centrifuging the homogenate at 105 000 x g for 1 hour.

Thus cytosol is a centrifugation term, (ie a fraction obtained by centrifugation)  and  ' should not be applied, in any context, to the intact cell' (Clegg, 1983).
The cytosol  may roughly be though of as the 'soluble' portion of the cellular extract obtained after everything else, including the microsomes, have been sedimented. (For those not familiar with subcellular frationation, centrifugation at 100 000 g for 1 hr is the 'standard' method of sedimenting microsomes. If your enzyme is found in the 100 000 g supernatant fraction, you can be  pretty sure it is soluble).
When we are referring to the cellular aqueous fluid  that 'holds'   the organelles and other  components we should use the term cytoplasm.
At the bottom of Clegg's article, the editors of TIBS have supplied the following quote, attributed to F.H.C Crick & A. F. W Hughes (1950):

If we were compelled to suggest a model for the structure of cytoplasm we would propose Mother's Work Basket -a jumble of threads, beads and buttons of all shapes and sizes, with pins and threads for good measure, all jostling about and held together by "colloidal forces".'

In being a  centrifugation fraction,  the term  'cytosol' is very like  microsome: the intact cell contains neither cytosol or microsome.
Ref
Clegg, J. S. (1983) What is the cytosol? Trends in Biochemical Sciences 8, (Dec, issue 12), pp 436-437

Per my bio textbook, they have cytoplasm as "the region contained within the plasma membrane" and cytosol as described as "site of many metabolic pathways" and "the region of a eukaryotic cell that is inside the plasma membrane and outside the organelles."
Ref
Brooker, R. J.; Widmaier, E. P.; Graham, L. E.; Stiling, P. D. Biology; McGraw-Hill Education: New York, NY, 2017.


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What causes leaves to be hydrophobic?
In my garden, I'm growing broccoli. I was spraying it with water the other day, and I noticed that water bounced off the leaves. When I just misted it instead of a full-on spray, the water beads collected, but stayed as beads instead of spreading out. Some of them bounced off, but some accumulated. So what makes that happen? I know the leaf is hydrophobic, but I haven't found by searching Google if there's a coating of some type on the leaf or if it's something else that's making it hydrophobic.

This is due to presence of a hydrophobic chemical called as cutin present at the the aerial surfaces of plants.

Cutin is one of two waxy polymers that are the main components of the plant cuticle, which covers all aerial surfaces of plants. The other major cuticle polymer is cutan, which is much more readily preserved in the fossil record,.[1] Cutin consists of omega hydroxy acids and their derivatives, which are interlinked via ester bonds, forming a polyester polymer of indeterminate size.

Source: https://en.wikipedia.org/wiki/Cutin

While your information on Cutin is correct, the effect described by the OP is due to extracuticular wax, not cutin itself. It is actually quite fascinating how long the nature and microstructure of these waxes and their relation to hydropobic surface effects was ignored. It's worth checking out the webpage of the research group working on the Lotus Effect: http://www.lotus-salvinia.de/index.php/de-de/ .


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Why does spraying water on plants help them survive in case of frost?
I've heard that spraying water on plants will help them survive the frost. Why is that?
Some say that you should do it in the morning right before the sun rises, and others spray water the whole time of low temperatures.
What is the explanation for why this spraying techniques works?

The question has already been asked in Physics.
According to the information there and here the sprinkling must continue throughout the period when temperatures are below freezing, and is only effective for temperatures down to around -5 °C.
Explanations invoke three interrelated effects: when water freezes heat is released so there is a warming effect; the temperature of an ice-water mixture is 0 °C; and an ice layer will insulate the leaf. As long as the temperature of the leaf stays above freezing there will be no frost damage.

Thanks, this sounds logical. But take a look at this answer: https://gardening.stackexchange.com/questions/33070/to-water-or-not-to-water-a-plant-right-before-near-frost-temps-in-mid-spring#answer-33075. It appears that fast thawing also plays some role here


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In what reaction of mitochondrial respiration is hydrogen peroxide an anomalous product?
I understand that hydrogen peroxide is produced in an anomalous manner during mitochondrial respiration, which also produces other by-products or free radicals. Does anyone know the details of the specific reaction in which hydrogen peroxide is formed and what is the normal product(s) of the reaction?

The normal product of mitochondrial respiration is water. Perhaps "incomplete reduction" would be a better phrase than "unpaired reduction".

Perhaps rare, but I think that's exactly what cytochrome c oxidase does.

I found your question unclear, which is why I have voted to close it. I do not think merely asking about the product is sufficient to justify it so I have changed it to ask for the details of the reaction (which will include the product).

I'm sorry but I have modified the question to make it more comprehensive. If you can expand your answer, with links to supporting references, please do so.


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What are these bumps on tomato stem?
What are the bumps on this tomato stem? They are way off the ground so I doubt they are air roots.
What are they, what function do they have and why do they form?

Those bumps are aerial surface hairs, a type of trichome. They are epidermal outgrowths.
Therefore it's vines are of pubescent type.
In addition to facilitating better exchange of gases, it also facilitate the vining process, turning into roots wherever the plant is in contact with the ground and moisture, especially if the vine's connection to its original root has been damaged or severed.

Sources:
1:https://en.m.wikipedia.org/wiki/Trichome#/search
2:https://en.m.wikipedia.org/wiki/Tomato

I'm very skeptical of the claim that these trichomes facilitate gas exchange or vining, or become roots. The long spiky trichomes are almost certainly for defense. The shorter fuzzy trichomes may serve to increase the air boundary layer, thereby decreasing moisture loss, but one can see that many of these shorter ones are gland-tipped, so they are probably also involved in defense. Trichomes come from only the outer epidermis cells, so they themselves wouldn't "turn into roots", though they do come from a similar developmental process as root hairs, which may explain the confusion.


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Do Japanese have a different pelvis position than Europeans?
I was watching a show that made the claim that European women's pelvis is tilted more forward compared to Japanese women's which places their butts higher up.
Is this information accurate?

It's probably best to not assume that anatomy in anime is accurate.

While the context of the question is "un-scientific", the question itself is neither off-topic nor opinion-based. The question is clearly asking about anatomy of human pelvises which can easily be answered scientifically. Those that are close-voting need to check yourselves and review what constitutes "off-topic" and "opinion-based".

I removed where I heard the claim from.

Which makes your claims even more "opinion based".

@Chris, it's not "my" claim and how is it even opinion-based? I heard something from a television show and I want to know if there are any studies to support the statement made by the source. This is not an opinion based question because studies can prove whether or not there are differences in pelvic positioning between populations.

According to this study there are significant pelvic position differences between Caucasian and Asian populations. However the biggest difference is lumbar lordosis (the curve at the small of the back) where Caucasians have almost 10 degrees more curve. The study doesn't explicitly say it but that would suggest Caucasians butts are higher.

Well well well what do you know! They were right!


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What is the name of this spikes insect?
Location is South India.
Behavior: It is not moving.
Month: May,
Place: No people come. (Actually species chooses the place on my next door, where neighbors left 2 months ago)

Can you add some more details? Location, type of habitat, size, how long it has been there, do you see them often etc.

@arboviral I added new HD image, is that quite enough to ID the species?

The Creature is "Debris-carrying Lacewing.".

(Source)

Attention: I get a high-risk warning when clicking the link!

@AlexDeLarge Same for me

Well then, I'm not going to click on it...


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Rosette formation: in which order are leafs created
From the picture below, it seems that new leaves are formed something like this (if you imagine the plant as a regular, 12 hour clock):
new leaf at 12 o'clock, then at 7 o'clock, then at 2 o'clock, then at 9 o'clock, and so on.
I imagine it could be some things as simple as 'always add 190 degrees'. Are the exact rules for this documented somewhere for various plants?

Spiral Phyllotaxis and the Golden Angle
The disposition of the leaves in your picture is not as simple as it seems. That's a spiral phyllotaxis, which can be very complicated.
The plant in your image is a houseleek, a plant from the Genus Sempervivum.
In those plants, according to Jeremy Burgess (Introduction to plant cell developmnent):

... leaf primordia are separated from each other in an angular arc that approaches 137°.

By the way, 137° is (almost) the golden angle (φ).
Here is an image explaining the phyllotaxis of Sempervivum (from Burgess, 1989):

Even more interesting is the pattern made by the 137.5° GA spiral of Aloe polyphylla:

Sometimes this can produce invisible spiral patterns, a phenomenon called parastichy:

Source: Burgess, J. (1989). An introduction to plant cell development. 1st ed. Cambridge [etc.]: Cambridge University Press.
PS: I know that this is off-topic, but I'd like to share this video from Cristóbal Vila, which deals with Fibonnaci sequence, golden ratio and golden angle in nature. Look at the flower disposition at 1:44 : https://www.youtube.com/watch?v=kkGeOWYOFoA

excellent, thanks! also thanks for the video link!


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Why is a gene for a fluorescent protein used rather than one for an enzyme that produces fluorescent molecule?
Green fluorescent protein (GFP) is a small protein that emits bright green fluorescence in blue light. It was first isolated from the jellyfish.
The gene coding for GFP can be expressed in bacteria, and so it is often used as a marker to show successful uptake of a gene by the bacterium.
What is the advantage of using the gene for GFP to produce easily detectable fluorescence, rather than using a gene for an enzyme that produces a fluorescent substance?
Ps. The original question I got was to explain about the disadvantage, which is that GFP may not fluoresce very brightly and so may be difficult to detect.
Thank you for your help.

Lemme ask you same thing, in reverse: what is the advantage of using a gene for an enzyme that produces a fluorescent substrate, rather than using the gene for GFP to produce easily detectable fluorescence? If you're getting something done directly, why do the same thing indirectly?

Possibly because some people discovered how to induce GFP before anyone discovered an enzyme route?  If indeed anyone has done that.

If you used a substrate you would have to get it into the sample. This would add variability in terms of penetration, reaction time and diffusion of the reaction product away from the site of interest. Why bother? Just image the GFP directly with none of this hassle.

GFP has a lot of advantages:

The detection of the fluorescence works directly and doesn't need a lysis step or the uptake of a reagent.
Fluorescence can be detected directly using a fluorescence or confokal microscope with the cells. This can be done while growing them on plates (works for bacteria and eukaryotic cell culture).
You can sort labelled cells using a flow cytometer.
direct tagging of proteins and their subsequent localisation on the cell is possible.
GFP is rather stable in the cells and not toxic.

To add to this: GFP will not diffuse out of the cells (or even out of a vesicle) and you can engineer cells to encode your protein of interest with GFP attached. You can even add all sorts of localization tags to GFP and observe where the tag leads your GFP.

There are no genes that I know of that encode proteins, more specifically enzymes, that will catalysed the production of a fluorescent compound from intermediates present in the average cell. Presumably one would need a whole pathway.
So I suspect that the question has never really arisen.

IIRC, pseudomonas fluorescens produces a carbon-scaffold molecule around iron ions which produces a fluorescent small molecule. But that would probably require expressing multiple enzymes


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I found this strange tooth in Galveston, Texas. What does it belong to?

I found this on May 7, 2017, on Bolivar Peninsula in Galveston, Texas. What's not visible are the treelike rings inside the tooth and what looks like a tiny interior porous center. It looks like it was considerably larger but broken off.
We're all taking bets on what it is!

Hi welcome to Bio.SE! Neat tooth! :). Could you please include an image from the top of the tooth if possible? Thanks!

Will do! It will just be a little later this afternoon.

My dentist said it was human's lower right first molar. I think it's starting to look like cow.

You should probably find a new dentist if they think that came from a human.

I'd agree that it looks bovine but there is a lot of homology in teeth so I wouldn't be confident in that determination, might at least be a ruminant though. See here for some bovine molars.

Sure, wishful thinking, but for its size it could be densiovan which would be awesome ... :D

@BryanKrause I agree that your cow tooth link looks very close.

@Bryan I think it has something to do with Bison. This link will take you to some fossil forums.

@Tytoalba Why do you think it is a fossil rather than a relatively modern tooth?

I didn't mean it is a fossil, I found these forums discussing about bovine (Bison) teeth, which can shade some light on this specimen. @BryanKrause

@Tytoalba Got it. I don't see a single tooth on there that is definitively attributed to a bison that looks like this one, though, is there an example I missed? I think it's more likely to be from common domestic cattle. People raise quite a few cattle in Texas, and there aren't very many bison there these days.

I didn't do a thorough research and I see it lacks the prominent stylid of a Bison. Never mind.

This discussion might help: http://www.nhm.ac.uk/natureplus/message/57652

This is a cow tooth. Your image matches above image.
https://www.flickr.com/photos/61377404@N08/12300347505

I agree with this answer. I grew up on a cattle farm and saw these quite often. But it would be important to know if cattle were ever raised on Bolivar Peninsula. It seems quite small.

Most likely a horse tooth. Check out this image from Wikipedia.

It doesn't look anything like any of the teeth in that horse's mouth. Compare to my link for a bovine molar in the link in the comments above.

It looks like a bison tooth
Just saying btw if u have any other bones post them in thefossilforum.com(gives little bit of help with fosills and bones)
How i identified it just search on tooth of random animal maybe you/ll see the answer somewhere


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Why does my gel have such poor resolution?
Brand new user to bio stack exchange here. I ran this gel (0.9% agarose, run starting at 60V then to 105V over ~30-45 min) with DNA samples containing 20uL of DNA and 1X tracking dye in each of the wells. I do not know why the resolution of this gel is so poor. I'm assuming it's from DNAse activity, as this is what my lab tech said it probably was. I'm pretty sure I did everything right regarding the procedure. I'm not sure what other info I could provide, other than the samples were prepared and stored at -20C a week prior to the gel being run. Here's a picture of the gel below.

Are you running the products of a restriction digest? How clean is the water that your DNA is dissolved in (e.g. nuclease free)? What size fragments are you hoping to see?

Yes, we used nuclease free water in the samples. I was expecting ~5.8kbp and 0.7kbp fragments in the second lane, ~6.8kbp fragment in the the third lane... I could go on to explain all of them if its necessary, but fragments were expected in each lane.

That your marker is also poorly resolved suggests that your gels system is the problem. Can you assign sizes to the marker bands?

@canadianer By marker do you mean my ladder in the leftmost lane? If you're asking for a picture of what the ladder sizes should look like heres a picture.

How did you set up your gel?

My diagnosis: no buffer added when the gel was cast. I see this every year when a class of students pours and runs gels.

@AlanBoyd My suspicion, too.

@AlanBoyd, oh, so using water instead of buffer? I always thought that made the gel just melt when voltage was applied. (Or so we've been warned)

Although your tech is referring to your DNA samples, your ladder also indicates there is some room for improvement of your running technique. -20C for a week should not have impacted the quality of the DNA assuming that it was good quality going into the freezer. You can mitigate DNAase activity by adding EDTA to your storage buffer, which will pull metal ions out of solution. Just make sure to take that into account if you're doing a reaction later that requires metal ions (like PCR).
DNA
Focusing first on the DNA samples. There are a few things to check.
How much did you load? I see you stated 20uL, but what was the concentration? It it more important to know the amount of ng being used as the sample. Various stains have different concentrations they can detect (EtBr, SYBR, etc.) I would check the specifics of the stain you're using to make sure you're loading an appropriate amount of DNA.
Are these PCR products? If so, how many cycles was your PCR run? I have seen similar results from PCR if the samples are run for too many cycles. Non-specific products begin to be produced in later cycles, and will cause degradation of your specific products. I would also re-check your primers, the extension time, and the polymerase you're using. It is more difficult to do extensions of the 5.8kb and 6.8kb sizes you mentioned, but not impossible.
Are these restriction digests? Do you have a control well showing the undigested plasmid, or other source? Your source should have a clean band first to expect a clean band in the results. If your source is clean and bright, and the digest looks like the samples above, check your digest buffer and enzymes.
Electrophoresis
There are several things which can improve the quality of an agarose gel. Thermofisher provides a guide for their tips and tricks. Below are things that I have found useful in my own experience.

The time between casting the gel and running it. A common practice is to make gels and store them in TBE/TAE buffer until they're ready to be used. In my experience, the quality of the gel will degrade over time, yielding diffuse bands. The best results are achieved with a freshly poured and cast gel.
Loading technique. Carefully loading the samples into the wells so that they settle as closely to the bottom without mixing with the surrounding buffer is key. The best results are achieved by having your pipet tip touching the bottom of the well, and slowly pulling it out as you release your sample so the sample does not have to settle down into the well on its own.
Run immediately after loading, and image immediately after running. Diffusion will cause nice tight bands to become poor the longer the samples sit in the well.
Voltage, timing, and agarose concentration. Getting these right takes practice. You'll want to try to run your gel as quickly as possible. The more time it sits in the gel, the more diffusion will occur. However, have the voltage too high, and you risk melting your gel. Vary the concentration of agarose to target the size of DNA you're after. I have previously used anywhere between 0.5% and 1.5%.
Prestaining the gel or poststaining? I prefer prestaining for the stains that work well, as it reduces the time the samples will sit in the gel allowing diffusion to occur.
I am looking at your ladder, and the link to the provided standard, and it is difficult to tell which bands are which. The 3.0kb fragment should stand out as the brightest, however the bottom band in your gel is the brightest. Is this the 3.0kb band? Maybe. It's difficult to count the number of bands above it to confirm. If it's not, which might be indicated by the fact that none of your samples seem to have run to the end of the gel, then this would be the 0.5kb band. If it is the 0.5kb band, the ladder intensity doesn't match up with your expected intensity. Double check your ladder so you can know what sizes you're looking at.


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Fastest observed biologically evolution rate?
Fastest possible evolution rate?
What is the theoretically quickest evolution rate?
For example, I could calculate this as the number of offspring an E. coli colony can generate at once * (time frame/time per generation) * mutations per generation, and then assume every organism on earth had this same evolution rate.
Is there a generally accepted value, perhaps based on mass of organism?

Without an explanation for how you are defining "rate" I think this question is fairly meaningless and I suspect it might be rooted in a misunderstanding of the term "evolution".

@BryanKrause Fair point.  I can describe what I mean in terms of a simplistic model.  If we use a binary string to represent DNA, there is a space of finite length binary strings that we can explore through mutation, crossover and selection.  From an initial starting population, and using biologically plausible parameters, what proportion of the space can be explored within a certain time delta?  Is this rephrasing clear enough?  If so, I'll replace my question.

I sometimes like to share this comic in circumstances like this - I don't mean any offense, but I think it sums up the problem nicely if you approach it with an open mind. My point is that a simplistic model will never capture "evolution" because evolution is an incredibly broad theory encompassing many separate parts. For one, although it's reasonable to consider finite length binary strings, biology won't produce genomes of the same length, so you need to consider strings of varying lengths. You very quickly get to a combinatorial explosion.

And although people often talk about "random mutation" the mutations in biology aren't purely random. You often have duplication of entire segments creating multiple copies of the same protein which can then diverge from each other. Further, mutation is only one tiny part of evolution, you also have selection, which is incredibly dependent on environment, and non-selective changes like genetic drift.

@BryanKrause I'm not saying the model is comprehensive, but there surely must be a way to mathematically model evolution rate according to some definition or another in a field over 150 years old.  All I was doing is offering one simple model to define rate, I'm sure someone has invented a better one.

@BryanKrause I've updated my question with an explanation of how "rate" is defined.  Can it be removed from hold?

As Remi.b already pointed out, if you allow fitness and phenotype to vary sufficiently, you could state that the rate of evolution is effectively infinite: complete in one generation. So no, I think it is still a poorly defined question.

I happened to notice this previous question in the sidebar of a question unrelated to yours, but I thought it might be of some use to you. The question is on selection but the answers get a lot more broad. You won't find a precise answer to your question but it might help you as a starting point to how people have attempted to model relatively abstract evolutionary processes. Like I was alluding to with my cartoon link, though, this is an entire field of work.

@BryanKrause, is an infinite evolution rate scientifically plausible?  I'm doubtful.  Anyways, I've simplified my question per Remi.b's suggestion.  Can it be taken off hold?

See How fast is fast? Eco-evolutionary dynamics and rates
of change in populations and phenotypes I think this what you were asking about

Theoretically, it really depends how crazy you want your model to be! Also it depends what you mean by "evolution rate".
Let's consider a very simple and quite crazy model. Let's assume that by evolution rate you mean the difference between mean phenotype between one generation and the next. Let consider a trait (which heritability is $h_N = 1$) which takes only two values $x_1$ and $x_2$. In a given generation, half the individual carry the trait value $x_1$ and half the trait value $x_2$. If the relative fitness of $x_1$ and $x_2$ are 1 and 0 respectively, then the evolution rate is simply $| \frac{x_2 + x_1}{2} - x_1 |$. Allow $x_2$ and $x_1$ to be very big values and the rate of evolution will be very fast. In the most extreme case, $x_1 = \infty$, then the evolution rate is simply infinite.

The model needs to incorporate mutation so we don't need to assume the traits already exists in the population.  It also helps if there is biological plausibility to the model.

@yters How is there no biological plausibility to the model? For mutation, simply do not assume x1 and x2 are held by half of the population.

@yters The amount of biological plausibility is up to the one that answers. My point was to highlight the question made little sense for this reason. If you ask "In theory, ...." you have to get ready to get an answer that is not practical. Instead you could ask "What is the fastest fastest evolution ever observed?" But then and again, you will really need to define what you mean by "evolution speed".

@Remi.b, what is a good definition of "evolution speed"?  I have no preference in the matter, I just want a good working definition that has evidence behind it.  Not being a biologist, I do not know the correct technical terms that will get an answer, so asking me for the correct technical terms is not something I can provide.

Talking about genetics, some may like to use the rate of neutral substitutions as a measure of the speed of evolution. Talking about phenotypes, some may like to use the Darwin (unit) to measure speed of evolution. Some may like to talk about speciation rate. In all of these cases, you cannot really ask for a theoretical limit without specifying exactly the basis for the model you wish to consider. You can ask though for observed evolution speed. Coming to phenotype, you'll have to specify whether plasticity counts as evolution or not.

I note that the question was edited/changed substantially since this answer was given, making it look off-topic now, although it was addressing the original question "What is the theoretically quickest evolution rate, that maintains biological plausibility?", not the current one, which asks about observed evolution.

Sure, we typically ask OP not to change their question after it has been answered. So, I edited the question back to what it was when I answered. If the OP has another question he/she must ask it on a different post. Thanks @Fizz for highlighting this issue.


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Chief Sensory Cells
What makes the second order neurons of posterior grey horn of spinal cord to be called as "chief" sensory cells?
Why don't we call 1st order, or third order neurons or other second order neurones in different part of spinal grey part as "chief" ?

Eh, searching on Google a bit, this terminology seems limited to two Indian sources: one textbook and one study guide, and isn't used anywhere else. There is a different area called the "chief sensory nucleus" which is separate. It just seems to be an attempt by those couple sources to refer to the cells which aren't one of those other categories. It isn't meant to indicate some special significance for those cells versus cells at other hierarchical levels, rather simply trying to classify different cell types within the spinal cord.


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Why would a human female have a sexual display despite male biased operational sex ratio?
why would a human female have a sexual display despite male-biased operational sex ratio?
In human society there is a male-biased sex ratio, due to female child rearing, which results from anisogamy. Human females sometimes expend great amounts of energy and resources performing display acts and doing things to attempt to improve their apparent quality to males. Human males tend to be eager, despite a certain level of socially imposed monogamy, and many males will mate with a low quality female. Why do human women do sexual display behaviors, when there are so many eager males to choose from?

Your question is not clear. Can you please add some more details to clarify it?

@WYSIWYG did my edits clarify enough/at all?

@WYSIWYG What is unclear about this question? Seems perfectly clear to me. Although I think more recent research would question the basic premise of human operational sex ratios being purely male biased, but I think we've agreed in meta not to oppose questions based on incorrect premises (and likely a good answer would address that possibility).

Okay.. I understood the question but I guess what you are talking about is a recent phenomenon and is not likely to be shaped primarily by evolution.

Because it is not just about mating and sex. Evolutionary it is also about care and bringing the offspring through life together.

Sexual arms race.
There is a fine and internally consistent theory that this strategy by females evolved to oppose the strategy of infanticide by males.  Males of many species including primates and possibly humans can increase their own genetic fitness by killing infants that are not their own.  This frees up attention and physical resources of the female to instead have the baby of the infanticidal male.  Lions are famous for this.  But this is in opposition to the genetic fitness interest of the female, who just invested a bunch of efforts gestating and rearing an infant who was then killed.
My favorite writer on this is Sarah Hrdy.  From the Wikipedia article on this\

This is where the idea of sexual counter-strategies comes into play.
  Hrdy theorized that by mating with as many males as possible,
  particularly males who are not part of the colony, mothers are able to
  successfully protect their young, as males were unlikely to kill an
  infant if there was the slightest chance that it might be their own.

This explains why women have the sexual displays referred to in the OP.  Other aspects of female human biology match.  Humans keep big breasts so they always look like they are lactating (compared to other animals) - to keep males guessing.  There is no external sign to indicate when a human is ovulating.  Females of other species are receptive and mate when they are ovulating - humans can mate any time.
A strategy of keep the guys guessing.  If one time he had sex with a given female, probably he shouldn't kill the kid.  Maybe it is his?
An interesting (& extremely arguable!) corollary to this is the premise that human culture in its entirety is the male countermeasure to this prehistoric female defense against infanticide: that male dominated culture is a method to ensure paternity.


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How does receptor downregulation/upregulation work?
My understanding is that if a cell is flooded with a certain neurotransmitter, it may decrease the density of that neurotransmitter. What I don't understand is how.
Is it a direct physical result of the receptor-ligand complex being internalized? I.e., the receptors simply aren't there anymore, because they've been internalized?
Or, does the internalization of specific receptor-ligand complexes actually get sensed by the cell somehow, causing it to produce fewer receptors in the future?

Both internalization (sometimes with degradation) and changes in gene expression can occur; the circumstances leading to the down regulation determine which (or both). It isn't necessary for receptors to be bound to their ligand to be internalized, though, and it isn't the internalization of receptors that causes changes in gene expression (I suppose it is possible that happens someplace, but not that I am familiar with). The processes involve activation of second messenger systems and kinases that either phosphorylate/dephosphorylate the receptors to mark them for internalization and/or degradation, or activate/deactivate transcription factors.
Here are two reviews with more information: one is newer but focused on a single class of receptors and fairly in-depth; the other is a bit dated but more broad, but brief:
Williams, J. T., Ingram, S. L., Henderson, G., Chavkin, C., von Zastrow, M., Schulz, S., ... & Christie, M. J. (2013). Regulation of µ-opioid receptors: Desensitization, phosphorylation, internalization, and tolerance. Pharmacological reviews, 65(1), 223-254.
Tsao, P., & von Zastrow, M. (2000). Downregulation of G protein-coupled receptors. Current opinion in neurobiology, 10(3), 365-369.
You can also read about long term depression, which is different from homeostatic responses to ligand concentrations, but it does seem to serve a homeostatic function to keep overall synaptic strengths from growing indefinitely, and the molecular pathways are very similar (and it is a very well-studied phenomenon so you will find a lot of accessible information).

> internalization of receptors that causes changes in gene expression
EGFR translocation to the nucleus was an example that came to mind (ref).

@CMosychuk Thanks for the comment, it's a good opportunity for a clarificaiton. Yes of course, there are receptors for which internalization itself (after binding a ligand) is a signalling mechanism. I was referring only to the homeostatic regulation of membrane receptor concentrations in response to excess ligand, as in the OP. I wouldn't consider receptor internalization as part of a regular signalling pathway to be part of that homeostatic regulation. But thank you for pointing out that internalization can be a signal, I didn't mean to imply that it isn't elsewhere.


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What plant is this? Edible, tastes like cress
My girlfriend got this at a Turkish supermarket in Berlin. It tastes like garden cress or a bit like radish. I looked up cress varieties but couldn't find this particular leaf shape.

you might get a faster response from the cooking exchange called Seasoned Advice

I think this resembles some sort of radish (german 'Radieschen') ... Different cultivars have quite some variety in terms of leave shape, so it is difficult to tell.

@John that was a very good idea, people there suggested a variant of watercress which it most probably is. https://cooking.stackexchange.com/q/81309/7718


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Does science have an explanation of how the first "common ancestor" formed in evolution?
I always have this question on my mind and I need a better explanation on this. Does Charles Darwin's theory explain it or are there any other theories which explain it better than Charles Darwin's theory?

This is a very broad question you will have to narrow down. Are you asking about  molecular mechanisms of evolution or the molecular development of an organism following fertilization?

Molecular mechanisms of evolution

Which Darwin theory? I suggest doing some research and improving your question with more information and demonstrated effort to answer the question

Let me explain it further, as we all know we all were descended from a single common ancestor. I just need a better explanation on how the first common ancestor had formed before the evolution occurs

The you are looking for Abiogenesis not evolution, you need a replicator before you can have evolution.

@hamilthj I don't see how "molecular mechanisms of evolution" is any better than what user54581 wrote originally. I don't know what "molecular mechanisms of evolution" means but if I had to guess I would guess the mechanisms of DNA mutation, not abiogenesis (which doesn't involve mechanisms of evolution, or at least insofar as evolution is involved it's not the hard part that makes it an actual question) and definitely not "how an organism is formed on a molecular level".

Darwin's theory of evolution (and the modern theory of evolution) explains how the current diversity of life developed. Remember, the title of Darwin's book is On The Origin of Species, not the origin of life.
As for how the current diversity of life developed, or how species originate, the theory of evolution states that life forms change and diversify gradually, and species arise and differentiate from related species, via the processes of random mutation at the time of reproduction and natural selection. The ToE is a complex set of theories with many different semi-independent aspects but that's what it basically comes down to.
Clearly all this requires life, or imperfect reproduction at least, to exist; it says nothing about the first life, and it cannot say anything about it because given what we know of the processes that lead species to arise and life to diversify and aquire its form, those processes cannot possibly have been in play when going from abiotic stuff to the first living systems.
In other words, the Theory of Evolution is how life develops once it starts existing; it would work equally well if the first life appeared via natural chemical processes or was created by alien tinkerers or the result of a time paradoxical sandwich dropped in the wrong place on primordial Earth. The study of how life could start existing is usually called "abiogenesis".
The issue isn't actually as clear-cut as it may seem, since there is a very wide unknown space between what we consider the most archaic forms of life, and any entity that could plausibly arise via purely abiotic processes; every theory of abiogenesis does assume that a lot of the features we consider essential to life must have arisen after some kind of replication appeared, meaning those features would have evolved. So there definitely is some evolutionary biology involved in investigating abiogenesis, and maybe if we ever solve abiogenesis it will be folded into the ToE (like I said, the ToE is actually a complex set of theories and observations, not one single thing. So while our understanding of what the theory says and can say currently excludes abiogenesis, our understanding and definition of the theory could evolve). But we haven't, and it currently isn't.
You need to edit your question however, because it is completely unclear from the title or text that you are asking about abiogenesis. Your question sounds like it's about embryonic development or biochemistry. Those are the current instances we have of organisms forming; whatever processes were at work in creating the very first life, well for one thing maybe we wouldn't want to call whatever that was an "organism", but more to the point those processes cannot happen today. The atmosphere is wrong and too full of oxygen, there are organisms everywhere vaccuuming up whatever resources those original biochemical processes might have used, basically there is likely no chemical environment on modern Earth that's anything like the chemical environment life originated in.
To answer your question though, abiogenesis is currently an unsolved question, so no, Science does not have an explanation of how the first organisms formed. But if you want to have an idea of how things could have happened, what the challenges are in figuring things out, and what things Science currently considers likely or impossible, there is a lot of active research in the field and many different hypotheses. The Wikipedia page for Abiogenesis has a fairly comprehensive rundown on this.
This video describes one of them (my favorite and the first I've found actually convincing, I have no expertise whatsoever to base this on but I plug it anyway; if nothing else it gives an appreciation for what kind of things the researchers in this field look at when thinking abiogenesis) :
https://www.youtube.com/watch?v=av98Brx23_4
(disclaimer: youtube throws up an error for this video for me right now but I've watched it before, I don't know if the video's down or if the problem's on my end)

Thanks for the explanation. Your explanation leads me to the next level of the theory of evolution

Darwin is quite explicit that his theory does not attempt to answer the question of how life originated.  Rather, it takes one (or a few) original forms as a starting point, and explains how diverse species arose from that start.  In his own words:
"Thus, from the war of nature, from famine and death, the most exalted object which we are capable of conceiving, namely, the production of the higher animals, directly follows. There is grandeur in this view of life, with its several powers, having been originally breathed into a few forms or into one; and that, whilst this planet has gone cycling on according to the fixed law of gravity, from so simple a beginning endless forms most beautiful and most wonderful have been, and are being, evolved."


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Can emulsion test be used to detect phospholipids?
The emulsion test- causes a white cloudy colour when lipid is dissolved in ethanol and then water added.
Can this be used for phospholipids? I am aware that they are polar so may arrange in a circular formation in water but would the test still work?
Thanks

Yes, the test will still work. And you are correct about the phospholipid's process of forming 'circles' in water. The reason the test still works is because alcohol increases the permeability of the edge of these circles by making them less structurally stable. This then allows the ethanol to enter.
The hydrophilic phosphate head is not soluble in alcohol as it is not a lipid, but after the alcohol can bypass these heads, they can interact with the inner hydrophobic 'tails', which are soluble. The white emulsion/layer will then form.
This can be seen in the experiment of using alcohols to test the permeability of cell membranes. -See this investigation carried out by Westminster College.


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Bird diversity and the avian flu
From Learning from the Octopus 1 (p. 201):

A complimentary line of defense would be to lower the chance of infection by lowering the prevalence and virulence of diseases…just keep the variability of nature intact…West Nile virus increases its prevalence when bird diversity declines.

and on p. 212:

A high diversity of bird species has recently been shown to be a key factor in reducing transmission of some diseases such as avian flu.

Why is this so?
What does bird diversity have to do with reduced disease transmission?

Welcome to Biology.SE. This is an interesting question! I edited the quotations in your question to make them more clear. Could you please provide a reference to the book (authors, a link) you are citing from? Thank you!

Biodiversity is the opposite of monoculture, and we know that one possible consequence of monoculture is disease transmission -- bananas being the modern poster child for monoculture leading to disease spread.
The concept seems to have been most clearly presented in
Schmidt, K.A. & Ostfeld, R.S. Biodiversity and the dilution effect in disease
ecology. Ecology 82: 609–619 (2001)

A community of abundant alternative hosts with reduced competence mitigates Lyme disease risk in this system by decreasing the average infection prevalence of ticks. When alternative hosts have net negative impacts on the most competent reservoirs, via competition and predation, the dilution effect is compounded. We believe this dilution effect to be a general phenomenon of disease ecology because the majority of vector-borne zoonoses are characterized by the fea- tures necessary for it to occur.

There are many articles following up on this one, such as Declining ecosystem health and the dilution effect:

The “dilution effect” implies that where species vary in susceptibility to infection by a pathogen, higher diversity often leads to lower infection prevalence in hosts. For directly transmitted pathogens, non-host species may “dilute” infection directly (1) and indirectly (2). Competitors and predators may (1) alter host behavior to reduce pathogen transmission or (2) reduce host density. ... Our study provides further evidence for dilution effect ...

However, not all agree that this is a general or even a real effect.  For example:

How changes in biodiversity alter the transmission of infectious diseases is presently under debate. Epidemiologists and ecologists have put a lot of effort to understand the mechanism behind biodiversity–disease relationship. Two important mechanisms, i.e. dilution and amplification theories have in some manner made it clear that biodiversity and disease outcome have an intimate relationship.... We suggest a multidimensional approach whereby the same disease system needs to be studied in different ecological zones and then the effect of biodiversity on disease outcome needs to be ascertained. Nonetheless, caution is to be taken while jumping to any conclusion as biodiversity–disease relationship is a multifactorial process.

--Does alteration in biodiversity really affect disease outcome? – A debate is brewing
The book seems to be making the specific claim that biodiversity reduces transmission of avian influenza, and without a reference I can't evaluate that, but I couldn't find any articles supporting the claim. I'd be skeptical about that claim without some good  evidence, because avian influenza viruses are exceptionally good at crossing species barriers, so biodiversity should be much less of an obstacle for them than more species-constrained pathogens.


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Global database for patients with rare and important injuries or disease?
I was recently reading Christof Koch's The Quest for Consciousness, and several times he mentioned how important some patients with sad and terrible brain injuries were for the understanding of the working of the brain.
It made me wonder how brain researchers as Koch and others find such patients. I expect that only a small number happen to see an expert-brain researcher who understands that this patient could be important for brain research, especially for such people in less developed countries.
More generally, I wonder the same for patients with very rare injuries or diseases, which could potentially be significant for medicin- and biology-research:

Is there a global database for patients with very rare deseases or injuries, making it possible for medical experts in the field to find them?

Even if the expert can not help the individual person, I imagine that such patients could be very important for future understanding/curing of the injury/disease. I hope to get some literature references or suggestion.

Are you aware of the concept of medical confidentiality? If not, you might find it instructive to read https://www.bma.org.uk/advice/employment/ethics/medical-students-ethics-toolkit/9-confidentiality. Then perhaps you will realize why the answer to your question is no.

@David Thank you, but your answer is not complete I believe. 1., such lists could be created when the patients or their relatives agree. 2., somewhat related lists do certainly exist, such as for organ transplantations. 3. I know that several very rare cases have been well-documented in medical literature, so your argument do you apply there either. But I see your point, and it gives some necessary conditions for what I was wondering about. Thank you.

I guess the closest you can get to this are collections of case reports. Where, if you were extremely interested, you could contact the author of the case report and if you are lucky get in contact with the patient.

The Undiagnosed Diseases Network (https://undiagnosed.hms.harvard.edu) is similar to what you're looking for; it's not for injuries, but rather for rare genetic diseases. @David: there are well-established procedures for getting informed consent.

@RaghuParthasarathy — if you have an answer to a question please post it as an answer. Comments are intended for asking clarification or making  suggestions to the poster, as you will have seen when you clicked in the comment box.

The MatchMaker exchange project is a federated approach that allows clinicians to find matching cases based on genetic or phenotypic similarity, retaining patient confidentiality.

The Undiagnosed Diseases Network is similar to what you're looking for; it's not for injuries, but rather for rare genetic diseases.

I don't know whether there's a global database of the sort you're thinking of, but
Crowdmed.com is a website on which patients post their own obscure medical cases and post a bounty for researchers to try to solve them.

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


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Is 7-nitroindazole neuroprotective against meth because it oxidizes peroxynitrate?
So 7-nitroindazole (7-NI) prevents methamphetamine (METH) induced neurotoxicity AND completely prevents meth induced dopamine depletion, but doesn't prevent meth induced hyperthermia. Strangely, a different study said that its possibly because of 7-NID's ability to prevent hyperthermia, (however it is important to note that this study did not test body temperature), yet all the other studies say the opposite, that 7-NI doesn't prevent meth induced hyperthermia.
Keep in mind that colder enviromental tempratures significantly attenuated METH-induced neurotoxicity
Could the reason as to why 7-NI prevents METH induced neurotoxicity and dopamine depletion simply be because it oxidizes dopamine oxidizer peroxynitrite noting that non-meth induced hyperthermia also cause neurotoxicity and produces peroxynitrite while showing the same neurotoxicity markers as METH induced neurotoxicity such as nitrotyrosine?


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How are collagen fibers in skin aligned with respect to skin surface?
I read in one paper that collagen fibers in dermis are randomly oriented in direction with respect to the skin surface. I can't locate that paper now. However, I came across this paper that indicates that collagen is always aligned parallel to the skin surface (page 3). Which one is correct?

Does epidermis have collagen?

Oops, sorry i meant dermis. Edited.

Collagen underneath the epidermis is not completely randomly oriented, in fact mostly they are directed along the muscle fibres beneath them.
This was first observed by Karl Langer and hence was given the name as langer's lines( of skin tension). This peculiar arrangement of collagen is responsible for maintaining integrity of skin at times of stretching force developed on them by the muscles. Had they perpendicular, then skin would tear easily.
This also has clinical relevance because during surgery if an incision is made along these lines the scar would be minimum.

Source: https://en.m.wikipedia.org/wiki/Langer%27s_lines

Great answer! Does this vary with age?

I don't think so


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What is methamphetamine's transport carrier across the BBB?
Which carrier protein allows methamphetamine to cross the blood brain barrier? I would assume it's SLC22 and possibly SCAMP1


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Why does the mass increase in this question?
So, on 'http://filestore.aqa.org.uk/sample-papers-and-mark-schemes/2016/june/AQA-BL3HP-QP-JUN16.PDF', question 1.b., they show a partially permeable bag of glucose solution, in a less concentrated solution. Since sugar is more dense than water, why does the bag get HEAVIER, when there's more sugar, and less water?

Hint: the bag is partially permeable, but to what?

You try to explain why you find it surprising that the bag would get heavier but I still don't understand your reasoning. I don't see how you go from the density of sugar and water and how much of them there is in the bag, to being surprised the bag is heavier. Maybe you could give more details on the logical connections there?

@DevonRyan If it's not permeable to sugar molecules, then is the amount of sugar inside and out remaining the same? If so, and water is going inside the bag, then the bag is swelling. Does diffusion do this? Make things swell? My understanding was that you couldn't create pressure this way.

@RozennKeribin If you replaced the sugar in the bag with water via diffusion, the bag would be lighter. My understanding is this what is happening in the bag. Why is it becoming heavier?

@Piomicron thank you, your question makes more sense that way (you might want to edit your question to include that reasoning). I think you have it right in your answer to DevonRyan: the bag is permeable to water but not sugar. Could you elaborate on the objection "my understanding was that you couldn't create pressure that way"? Is there a specific source you are basing this on?

@Piomicron: Osmosis :)

@DevonRyan hey, I thought we were making them work through the answer and not just giving it! :p

@RozennKeribin I still expected Piomicron go from "osmosis" to why it'd result in the phenomenon, but point take :)

The reason that dialysis bag A and B will get heavier is due to water diffusing into the bags in order to bring the sugar concentration on both sides of the membrane to an equilibrium. Likewise bag C and D will get lighter as water will diffuse out of the bags in order to bring the system as close as possible to equilibrium. Water diffusion is also called osmosis and can be studied closer here: https://en.m.wikipedia.org/wiki/Osmosis


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What is sequential passaging?
I have read a journal that describes sequential passaging with the purpose of measuring resistance development in bacteria. I would like to know more about how the method works ie. what does "passage" mean?
https://www.nature.com/nature/journal/v517/n7535/pdf/nature14098.pdf, Methods part, under resistance studies

Can you please link the article?

The word "passage" in biological research methods generally refers to transferring a part of a culture (cell/bacterial/animal) from old medium to new medium.

I am normally reluctant to cite Wikipedia articles, however, the one for Sequential or Serial Passaging explains it quite nicely.
In short:

In microbiology, sequential or serial passaging refers to the process
  of growing bacteria or viruses in iterations. In essence this means
  that a virus or a strain of bacteria will be isolated and allowed to
  grow for a period of time. After the sample has grown for some time,
  part of it will be transferred to a new environment and allowed to
  grow for the same period of time.This process will be repeated as many
  times as desired. The final product is studied, often in comparison with the original virus or bacterial strain to see whether it has evolved or any other changes have occurred.


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What is the difference between pluripotent and totipotent cells?
Both develop into specialized cells.Then how are they different?

Have a look at https://en.wikipedia.org/wiki/Cell_potency. By the way, it is pluripotent.

@GerardoFurtado You can easily correct such spelling mistakes. That's why we have the edit function. And it is not seen as offensive here, as it helps to improve the question/answer.

Expending on Gerando Furtado link
Totipotent cells can differentiate into three germ layers (endoderm, mesoderm, or ectoderm), into cells of the cytotrophoblast layer or syncytiotrophoblast layer of the placenta.
Pluripotent cells can differentiate into the three germ layers (endoderm, mesoderm, or ectoderm).
So totipotent cells develop into the all the cells of the embryonic body and fetal side of the placenta. While pluripotent cells can only develop into cells of the embryonic body.


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What percentage of fish are herbivorous vs. carnivorous?
It appears that the majority of fish we eat are carnivorous, such as salmon and tuna. This got me wondering how common herbivores and carnivores are among fish species. I couldn't find an answer to this question through a cursory search of the internet.

I don't have an answer to this but there are a number of elements I think can be helpful for you in finding an answer.
First, a helpful word for searching here if you didn't know or hadn't thought of it is "trophic", as in "trophic level", as in "how high this organism is in the food chain".
Making searches related to fish and trophic levels I didn't find a single result for all fish; there are plenty of papers and graphs about the trophic distribution of fish but it's usually within a specific context or ecosystem. For example this graph gotten from Google Images, from a paper that looks at reef fish in Hawaii:

You can see in that graph, and plenty of other papers confirmed, that "herbivore/carnivore" may not always the most relevant distinction in terms of what a fish eats; unlike on land, where the base of the food chain is plants which are pretty big and visible and so are most of the organisms that eat them, in the ocean the base of the food chain is phytoplankton, which is eaten by zooplankton, both of which are what most of the fish we consider "at the bottom" of the fish food chain eat, so by that standard almost all fish are carnivores. But it doesn't seem to be how the word is used by everyone in the field; the graph in question being an example, distinguishing "Benthic carnivores" from "Planktivores" (Plankton-eaters) and "Piscivores" (fish eaters; presumably the "carnivores" eat non-fish animals).
See also this graph looking at reef fishes at various sites in the Caribbean:

Or this graph looking at the trophic structure in a stream

both of which similarly distinguish things more finely than "herbivore/carnivore".
And this, that I got from a search for "fish trophic histogram", ties the concepts to trophic levels (but on a local scale only again, this time the Mediterranean):

Otherwise the FishBase database seems to contain trophic pyramids but they need to be seen per ecosystem and there are a lot of available ecosystems, and given the shape of most pyramids they might include more than just fish.
As an aside, this paper might give a good explanation for why most of the fish we eat are carnivorous:
Trophic level scales positively with body size in fishes

I was indeed thinking pescivores/invertivores vs. herbivore/planktivore/detritivore. Very good information +1


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Larynx descent in male and female deer
Male red deer (Cervus elaphus) and Male Fallow deer (Dama dama) have a descended larynx, presumably for size exaggeration - to attract mates and intimidate other animals.

Does this descent occur after sexual maturation?
Do females of these species also have descended larynx?
In males, does this occur twice - just as it does with human males?
Do deer use size exaggeration to intimidate other animals, other male deer only or both?
Lastly, are there other typical behaviors associated with size exaggeration (i.e. standing on back legs)?

Thank you in advance. I attempted to search for these online but so far have not found any answers. Of course, any cite-able literature containing the answers would be ideal.

Welcome to SE Biology. This site attempts to build up a repository of questions and answers that can be useful to others as well as the poster. Thus, we discourage multiple questions in one. As your five parts are all about the same topic, this is not a criticism here, but I have edited your title to remove "5 questions about" so that the subject is clear and abides by our guidelines.

I apologize. The most important question is if larynx/hyoid descension occurs in both sexes. If someone could answer or point me to the appropriate literature for that I would appreciate it.

No need to apologize. I can't help you but let's hope someone else can.

Apparently not...

I’ve modified the title slightly and voted the question up to give it some more exposure. It may just be that this list doesn’t include the sort of specialist who could answer your question. Some areas (ornithology, for example) are more highly represented than others.

Thank you. Since posting I have finished reading "The descended larynx is not uniquely human" by Fitch and Reby. They conclude the larynges of male red and fallow deer do descend, although these animals have control, whereas we do not. They (deliberately) avoided does of these species which makes it difficult to contrast with human females (who have one post infancy descension for speech.)

Male mammals who use deeper mating calls are successful because it exaggerates their size. Researchers studied mating calls produced by 72 species of land mammal.


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Estimation of cell count of E.coli culture
Can I get some help with an estimation of a cell count in a culture of E.coli cells if we assume we begin with $10^6$ cells, that they divide every 30 minutes and they are incubated for 12 hours?
I do not know how to do the calculation with a start number that is not 2, if it was it would just be $2^{24}$. But how is it done when the starting number of cells is $10^6$?
Is it $(10^6)^{24}$?
Thank you!

You start with $10^6$ cells. After 30 min they double, so there are $2⋅10^6$ cells. After another 30 minutes they double again, so there are $2⋅2⋅10^6$ or $2^2⋅10^6$ cells. After three doubling periods, the number of cells is $2^3⋅10^6$. Doing this, the equation for exponential growth should become evident. All you must do now is determine the number of doubling periods in 12 hours.


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About cell membrane; action potential and resting potential
Ion X is negatively charged and more concentrated inside than outside the membrane potential of a cell
therefore Ex (equilibrium) is positive. Ion X is unknown.
Why is the equilibrium positive?

Assuming this is a homework assignment, we do expect OP to show prior research effort. At the very least you can provide the meaning of the acronyms used and a plausible way how you think the problem should be tackled. Good luck!

Possible duplicate of If the average resting potential of a neuron is -70 mV, why is there such a high ratio of potassium ions inside relative to out?

(note: the question isn't an exact duplicate, but otherwise it should be closed as a "homework" problem due to low effort; the principles addressed in the other question should help the OP, however)


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What is the difference between differentially expressed genes and deregulated genes?
Can anyone explain clearly what is the difference between differentially expressed genes and deregulated genes?

have you done some research on your own and if so, why it wasn't satisfactory?

Any gene whose gene expression differs significantly from some reference is considered to be differentially expressed. I think the most common representation of differential expression is the volcano plot, where you're plotting the fold change or log2 fold change against the -log10 p value assigned that gene.
This means a couple of things: One, you need a sufficently large sample size that you can actually get statistics, and two, you need a sufficient reference sample which will act as your baseline.
If a gene is degregulated, however, the expression is aberrant. In order to characterize aberrant expression you need a normal sample or accepted reference sample, and the sample of interest. This might be as simple as tumor vs normal tissue from the same patient.


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Dominance coefficient
I am trying to understand the meaning of the dominance coefficient. I'll be more specific to what I don't understand, in a moment.
Let $A_{11}$, $A_{12}$ and $A_{22}$ be genotypes with fitnesses $1$, $1-sh$ and $1-s$ respectively. I can understand the meaning of the selection coefficient $s$ as its sign clearly determines which allele is more advantageous.
Though, I cannot figure out the meaning of the dominance coefficient $h$. I understand the following:

if $h>1$ we have underdominance i.e. both homozygotes are more fit than the heterozygote
if $h<0$ we have overdominance i.e. the heterozygote is more fit than the homozygotes
if $0 < h <1$ we have that the heterozygote is only more fit than the deleterious homozygote

The last point is called incomplete dominance as opposed to complete dominance in the cases $h=0$ and $h=1$. Here, I'm having trouble to understand how this is related to dominance. I mean, I can clearly state that $h=0$ implies that the fitnesses of $A_{11}$ and $A_{12}$ are equal, but why does this imply that $A_1$ is dominant and $A_2$ recessive (the situation $h=1$ is symmetrical of course)?
For this terminology, I'm referring to Gillespie's Population Genetics: a concise guide. A table resuming what I'm talking about is also on Wikipedia here.
I'd like to point out that I'm not a biologist, but just a mathematician, so it may be something simple in how dominance works that I'm missing. Also, for the same reason, please, forgive me if I have worded something not appropriately. Thanks to those who will help.
EDIT: I'm not asking what the biological process behind dominance is. I'm just asking how $A_{11}$ and $A_{12}$ having the same fitnesses (which, for me, reads as having the same chance at surviving) relates to $A_1$ being dominant. As it was pointed out in the comments, this is the definition of dominance. Though, I thought that dominance of one allele means only which phenotype will prevail in the heterozygote case and I cannot find the relation between the two definitions.

The answer to I mean, I can clearly state that h=0h=0 implies that the fitnesses of A11A11 and A12A12 are equal, but why does this imply that A1A1 is dominant and A2A2 recessive  is just, because it exactly how dominance is defined.

If your question is about the mechanism behind dominance relationships (which seems to be what your last paragraph is asking for), then you should have a look at Why are some genes dominant over others? What is the mechanism behind it? and eventually Evolution of dominance of alleles.

Possible duplicate of Why are some genes dominant over others? What is the mechanism behind it?

Thanks for your comment. I think I'm just missing the big picture then. I thought dominance was only related to which phenotype will show. If fitnesses of $A_{11}$ and $A_{12}$ are equal, doesn't it mean just that $A_{11}$ and $A_{22}$ have the same chance at surviving? Isn't this what "fitness" measures?

Fitness is indeed some function of survival and reproductive success. The exact definition of this function may slightly vary depending on the model used.One will not that fitness is typically considered as a phenotypic trait. Note that when modelling fitnesses with $s$ and $h$, $s$ is typically positive and $h$ is typically between 0 and 1. For cases of overdominance, authors often prefer to use other 2 variables to express the fitnesses of all three genotypes. I am not sure this comment is of any help though...

Thank you for asking such a well-thought out question, I really enjoyed how hard this made me think about the concept. I think there might be an issue here that's quite common to biology, in my experience- poor definition of terminologies.
I think the core question can be summed up by your comment:

I thought dominance was only related to which phenotype will show. If fitnesses of $A_{11}$ and $A_{22}$ are equal, doesn't it mean just that $A_{11}$ and $A_{22}$ have the same chance at surviving?

In my thinking, the definition of dominant could mean two things:

The expression of a particular characteristic
The fitness associated with the expression of a characteristic

Of course, the second definition depends entirely on the first- if the phenotype of the heterozygote ($A_{12}$) is the same as the homozygote ($A_{11}$ or $A_{22}$), then their fitness must be the same- evolution acts on phenotypes, not genotypes.
Let me break this down using Gillespie's tables. For a given value of $s$ (between 0 and 1), we can imagine the following scenarios for the value of $h$:

$h$
Phenotype
$A_1A_2$ fitness
Dominance scenario

h=0
$A_1A_2$ phenotype = $A_1A_1$ phenotype
$1-s\times 0 = 1 = A_1A_1 fitness$
$A_1$ is dominant allele

h=1
$A_1A_2$ phenotype = $A_2A_2$ phenotype
$1-s\times 1 = 1 - s = A_2A_2 fitness$
$A_2$ is dominant allele

This is assuming the phenotype for $A_1A_2$ is the same as the phenotype of the homozygote, in each scenario. It may be possible that the phenotypes are different, but the fitness is the same- what we are actually measuring with $h$ and $s$ are fitness, not phenotypes. But if the phenotypes are the same, the fitnesses must also be the same- natural selection works on phenotypes, not genotypes.
Where the break between fitness and phenotype becomes complete is when $h$ is a value other than 0 or 1 (not complete dominance).

$h$
Dominance Type
Scenario

0<h<1
Incomplete dominance
The heterozygote ($A_1A_2$) more fit than $A_2A_2$ and less fit than $A_1A_1$

h<0
Overdominance
The heterozygote ($A_1A_2$) more fit than homozygotes ($A_1A_1$ and $A_2A_2$)

h>1
Underdominance
The heterozygote ($A_1A_2$) less fit than  homozygotes ($A_1A_1$ and $A_2A_2$)

In each of these cases, the phenotype of the heterozygote is something different than either of the homozygotes (hence the term incomplete dominance). What the value $h$ is measuring here is not the difference in phenotypes, it's the effect it has on fitness- which might be different in different contexts.
Let's think about the classic example of overdominance, sickle cell disease. In terms of fitness, individuals with one copy of the sickle cell allele have the sickle cell trait. The sickle cell trait offers resistance to malaria, and therefore higher fitness in regions with endemic malaria. An individual with two copies of the sickle cell allele are less fit because they have sickle cell disease. An individual with no copies of the sickle cell allele is less fit because they don't have resistance to malaria infection.
But this measure of dominance, where we define dominance as the fitness associated with a the expression of a characteristic, is context-dependent- individuals with the sickle cell trait are prone to other diseases, and in the absence of endemic malaria it might be they have lower fitness than an individual with no copies of the sickle cell allele ($0<h<1$).
If we think about dominance as simply the expression of a characteristic, we would actually describe the sickle cell heterozygote as co-dominant- when you look at the blood of individuals with sickle cell trait (heterozygotes), they have a mix of normal-shaped red blood cells and sickle-shaped red blood cells.
So to conclude:

Dominance sometimes refers to the expression of a trait in relation to an allele, and sometimes refers to the fitness associated with the expression of a trait in relation to an allele.
Differences in fitness imply differences in phenotype (because natural selection acts on phenotypes, not genotypes)
Differences in phenotype do not necessarily imply differences in fitness

I wrote also some notes on the following, but as they're not directly relevant to the question (but might be useful for Googlers later on) I will put them here below the cut:
Table of relative fitness measures with dominance coefficient $h$ and selection coefficient $s$

Genotype
$A_1A_1$
$A_1A_2$
$A_2A2$

Relative fitness
$1$
$1-hs$
$1-s$

The choice of alleles assigned to $A_1$ and $A_2$ are arbitrary- in reality these are As, Ts, Cs, and Gs. By convention the first allele is the dominant one, but if you're not sure which is dominant before you test it may be the second!
Similarly, by convention we assume the individual with $A_2A_2$ is not more fit than individual with $A_1A_1$ (in other words, $0<s<1$). But you might have it backwards!

More often than not selection acts at the phenotypic level, and dominance refers to the phenotype. However, when we talk about genotypic fitness ($W$), without any information about the phenotype that each genotype produce, we disregard phenotypic quantity and look at phenotypic quality (fitness). By saying that $W_{A_{11}}=W_{A_{12}}>W_{A_{22}}$, we assume that the phenotypic quality of $A_1$ dominates over the phenotypic quality of $A_2$ because $W_{A_{12}}=W_{A_{11}}$, and not $W_{A_{12}}=W_{A_{22}}$. But this is not always the case.
We cannot say that $A_1$ is dominant over $A_2$ because we don't have the information about the phenotype. Let's look at two scenarios. In scenario 1, we have a population in which the following genotypes produce the following phenotypes:
$$A_1A_1 \rightarrow GREEN \\
A_1A_2 \rightarrow YELLOW \\
A_2A_2 \rightarrow RED \\$$
Let's assume that this species cannot distinguish $GREEN$ from $YELLOW$ and these are also the colors that have the highest reproductive success, which means that the following fitness values can apply:
$$W_{A_1A_1} \rightarrow 1.0 \\
W_{A_1A_2} \rightarrow 1.0 \\
W_{A_2A_2} \rightarrow 0.9 \\$$
If we don't have the information about the phenotypes described above, one could mistakenly assume that $A_1$ is dominant over $A_2$ based on the fitness values only.
In scenario 2, assume the following phenotypes and fitness values:
$$A_1A_1 \rightarrow GREEN \rightarrow 1.0\\
A_1A_2 \rightarrow GREEN \rightarrow 1.0\\
A_2A_2 \rightarrow RED \rightarrow 0.9\\$$
In this case, assuming that $A_1$ is dominant over $A_2$ is correct, but one cannot be certain of that, unless we have the information about the phenotypes.

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


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Why can Toll-like receptors be found either inside and outside the cell?
Innate immune cells may present Toll-like receptors either inside (TLR3 and TLR9, for instance) or outside (TLR4 and TLR5, for instance) the cell, but is there any beneficial reason for this? If so, what is it?

When you say inside of the cell, do you mean in the cytosol or inside the  ER, vesicles, endosomes? Remember inside the cell can be many places so please be a little more specific.

By inside, I mean any compartment/region which is located within the cell.

TLRs are used to identify features that are typical of pathogens. Different TLRs tend to identify different features, so that a wide range of pathogens can be identified. Some of these pathogens may be extracellular (such as some kinds of bacteria that are recognized by TLR4, which is extracellular) and some are intracellular, like viruses (some of which may be identified by TLR7, which is intracellular).
The fact that innate immune cells have these is a little bit of a red herring, because they aren't limited to innate immune cells -- they're widespread among many cell types, and are effective at protecting the specific cell, not just activating innate immune cells.


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Origin of melatonin: oxidative stress defense OR circadian rhythm?
Question
Which functional role of melatonin came first?

Regulation of the circadian rhythm
Defense against oxidative stress
Other

Background
I was well aware of the important role melatonin plays in Human sleep behavior, and circadian rhythm regulation, quoting the Wiki page:

Melatonin, also known as N-acetyl-5-methoxy tryptamine,1 is a
  hormone that is produced by the pineal gland in animals and regulates
  sleep and wakefulness.2

What I was not so aware of, but now quite fascinated to learn about, is melatonin's role in oxidative stress management. In fact, the quote below is taken from the sentence immediately following the one above, in the same Wiki page:

it functions as a first line of defense against oxidative stress.3

Related Stack Bio Discussion
I also came across this Stack Biology answer to the question "Does melatonin change the appearance of humans?", quoting it:

Melatonin works as an antioxidant and helps in removing free radicals
  from the body ... I would have to conclude that
  melatonin could have a part to play in maintaining the beauty of your
  skin.


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Is there a defined non-trivial chromosome number distribution for a given kingdom?
I'm pretty aware of the mechanisms for chromosome number evolution in specific groups (e.g. inside a given genus). Nevertheless, looking at a broader scale (e.g. in the Metazoa kingdom), is there a well defined distribution for the frequency of occurrence of chromosome numbers?
For example, are species with small chromosome numbers more frequent than those with large chromosome numbers? If so, is there some sort of scaling relationship between number of species and number of chromosomes?

Page 445 for a start.

Not in my country...


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What is this compound-leaf tree in Southern India?
I am staying in South India. I didn't find any flowers to this tree; just leaves.
Just seeing the leaf, I am guessing Arabian Jasmine, but my tree doesn't have flowers or seed buds like Arabian Jasmine has.

I added more clarity image, is it ok to ID this plant ?

A clear shot of the whole leaf would be nice. Also a comment about where it's growing and how big it is would be helpful. Thanks.


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Does our brain emit any kind of waves?
I am currently trying to start a research project, and this is the most important question that needs to be answered. I cant't move ahead without knowing the chemistry of the brain.

brain waves [as per title] and chemistry [as per question body] are related but not identical. Tip: google 'brain waves' and see what pops up. The first hit is likely to be very useful. As of now this question is too broad and unclear. I would advise editing it to make it fit the conventions of this site.

Cells in the brain communicate with each other through electrical (and chemical) signals. The electrical signals from millions of neurons add up, and can be detected from outside the skull. This is called electroencephalography.
The signals that are strongest when measured in this way are often periodic or oscillatory (i.e. wave-like), because similar electrical signals from many neurons support each other if they are active synchronously. In contrast, when neurons are firing in a disordered way, then their electrical signals can partially cancel each other out when measured from outside the skull.


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During a large forest fire, what is the evacuation behavior of birds?
I'm interested in birds' behavior during large forest fires. Do they fly away as soon as they smell smoke, or wait until seeing fire itself? Do they fly away in flocks, or individually? Do they ever try to return to the area later, or just abandon it for good?
Interested mostly in average forest birds like jays, cardinals, finches, etc.

The exact behaviour of birds during a wildfire is unclear and there is little scientific evidence on their exact behaviour. Anecdotal notes from eye witness observations indicate that healthy birds fly away from the affected area before they are in danger. Birds that are unable to fly or move out of danger from the fire such as chicks in nest and indisposed birds are likely to die. Different species are likely to react differently to fire, species that flock normally will probably flock together as they fly and species that are more solitary are not likely to flock. Most fires happen in late summer and fall, just after the breeding season for most birds and during their migration, meaning they can escape the area. If the fire is very widespread, the birds may not be able to find appropriate shelter and food and would likely die as a result.
Wildfires are a natural phenomenon and birds have evolved to adapt strategies to deal with them. Some birds benefit from wildfires as they are a normal part of ecological succession.

Ecological succession is the gradual process by which ecosystems
  change and develop over time in response to a disturbance or
  colonization of new habitat.

Fire essentially creates a new habitat in which not all the same birds will use. Blue Jays prefer forests, but if a wildfire burns a forest, it will likely become a shrubby field afterwards and may take years to regrow into a forest. The Blue Jays will not likely return in large numbers until the habitat is a forest again.
A remarkable bird that is dependent on forest fires is the Kirtland’s Warbler. They breed in Jack Pine forests that are a certain height, once the forests mature; the habitat is no longer suitable. The jack pines themselves only release their seeds from cones in hot fires as they are serotinous and only open when exposed to intense heat, greater than or equal to 50 °C, the typical case is in a fire. The wildfires then create a succession cycle to always have suitable habitat for the Kirtland’s Warbler. Fire suppression of forests by humans has been listed as one of the reasons that led to large declines of this species.
Additional reading:
How Wildfires affects Birds?
Jack Pine Information

Very interesting that forest fires usually happen around the migratory season for birds. And the Jack Pine / Warbler relationship is fascinating. How would the seeds laying on the ground survive the fire itself? Does the Warbler eat the seeds and leave?

The seeds are not fire-resistant, but fire adapted. The Jack Pine cones have a waxy coat that protects them from being burned outright. The Jack-Pine cone can survive temperatures of 800F for 5 minutes. The heat melts the wax which allows the cone to open up, the seeds are not all released right away and there is a time period until they drop. They are adapted to drop after the fire has left the area, removing competing plants and putting nutrients in the soil. The Kirtland's Warbler does not eat seeds, only insects and berries, it relies on fires to regenerate new forest that it nests within.


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What is the name of this plant with 4-5 lobed leaves?
Location is India, It has 4-5 lobed leaves with flowers & pointy seed pods.

I am thinking it is Wild raddish.

50 mins still no answers, what more else details to ID this plant?. Image is not blur very clear.

please include the location of the plant and preferably some info about the surrounding habitat. Also, what are the sizes of the leaves and petals?  Do you have any closeup photos of the leaves or flowers? (Include this info by editing the question directly, do  not add it in the comments). Thanks.

Also, be patient. We're not some  sort of service -- we all have busy lives. But don't worry, when  you get your answer, it should be well supported

Looks like Asian spiderflower.

Thank You. It is Asian spiderflower

Yeah strongly looks Cleome viscosa, very common in West Bengal, too. Another species, C. rutidosperma that have 3-lobbed leaves and violet flowers, is also very common in India.

It is not member of radish family (brassicaceae) but it is a close relative of that.


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How do fishes "breathe" while eating?
First of all, a fish opens its mouth and water enters which passes through its gills. This helps in oxygenating its blood. So, if any food particle is in its mouth, how can it "breathe" i.e. how does exchange of gases occur? Shouldn't the pathway where water flows from mouth to gills be clogged like a drain full of sludge?

Food particles don't just sit around in the mouth; they go from the mouth to the stomach. I would expect most animals can survive a lack of oxygen intake for the mere seconds it takes for the food to move on. In any case, according to the Florida Museum of Natural History, fish generally do not chew their food, so the pathways should not be "clogged like a drain full of sludge".

They can pump water over their gills with their opercular flaps (i.e., the structure that covers and protects the gills). This is assisted by the branchiostegal rays. Food would generally not interfere with this process. Additionally, gill rakers assist in keeping food in the mouth.
Some great references for questions like this:
Barton, M., & Bond, C. E. (2007). Bond's biology of fishes. Thomson.
Moyle, P. B., & Cech, J. J. (2004). Fishes: an introduction to ichthyology (Vol. 726). Upper Saddle River, NJ: Pearson Prentice Hall.

Please update your answer by citing and/or summarizing supporting evidence from reputable sources. Thanks.

regardless of your own legitimacy, the internet doesn't know that about you (nor should users passing through necessarily believe that about you -- there are plenty of "fake" experts out there). Having a more formal source of info allows users to check in on the legitimacy of something more completely & objectively. It also enables them to use your source as a doorway to learning more about the topic. Take a look through Yahoo answers or Quora and see how many "legitimate" answers from "experts" are wrong -- without regular citing practices, users will never know one way or the other

I have added 2 sources, besides my own personal expertise as a fisheries research biologist

@theforestecologist You made a good point, thus, I have added to my response

Thanks very much. We're here to educate, so doing our best and most thorough job is worth that extra effort! :D.  +1.

Fish that are filter feeders generally have Gill Rakers which prevent food from actually damaging and clogging the gills.