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Deionized water - can it be beneficial for metabolic acidosis?
I ran into an interesting question today that examined the science around alkaline water and its advertised 'generalized health benefits' assumed to be (but incorrectly) stemming from a rise in blood pH. Logic behind the misassumption itself stemming from a rise in urine pH.
What I'm trying to figure out, is would deionized water (slightly acidic water) actually improve short term metabolic blood acidosis and ironically raise pH levels? Proposed ideas are 1) an acidic water stimulated elevation in bicarbonate secretion (kidneys and exocrine pancreas ) and  reabsorption (to circulation), 2) elevated mineral resorption or 'leaching' from cells. These don't sound all that great in themselves, but regarding a short-term net effect on pH (either on urine or a hypothetical blood ph), could not deionized water have a net alkaline effect due to bicarbonate regulation and cellular reabsorption of minerals being inherently 'slower' than the near instantaneous acid-base reaction?
Alkaline metabolic products of an acidic source that may be included in water (ie lemon) do not count as justifications to an answer. Only looking at water.
If anyone has any relevant studies, feel free to share them, I can't seem to find anything outside of fish.

I'm no expert in blood pH regulation, but it seems highly unlikely that you can treat acidosis by attempting to lower the pH further.  The normal treatment of (acute) acidosis is to give alkaline fluids, usually a bicarbonate solution.  Also, I wouldn't trust any information from the alkaline water peddlers -- it looks like a typical scam.  See for example http://www.quackwatch.org/01QuackeryRelatedTopics/DSH/coral2.html

Absolutely, as a scientist of metabolism I'm fully aware of the quackery in alkaline water. But, my question really is based in the idea: if bicarbonate water increases urine pH, this logically indicates an elongated systemic shift to lower blood pH. Perhaps, by causing a quick decrease in urine pH, an elongated shift towards increasing blood pH wouldn't be out of the question? (As you can guess I'm no expert in blood pH regulation either)

I don't think increased urine pH generally indicates a decrease in blood pH. It seems more likely that urine pH goes up when drinking alkaline fluids precisely because regulatory systems act to keep blood pH constant. Also, this is not a closed system, due to respiration CO2 exchange; and urine pH does not affect blood pH -- it's the other way around. Just some points to think about!

You're absolutely right in this regard, but I do feel there would be a window of a lower blood pH, as compared to baseline, following elevated excretion of alkaline minerals/chemicals/metabolites ect. And just by logic, an opposite effect in which increasing acidity of urinary pH may consequently cause systemic overcompensation leading to a more alkaline blood pH. All theory though, I can't find any definitive proof of this concept anywhere in any manner ("blood pH compensation causing or following a change in urinary pH")


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Can I do an MS in biotechnology after a bachelors degree in chemical engineering?
I recently graduated from high school and now have to make a decision about my undergrad major. I am interested in biotechnology but my parents suggested that I should opt for a broad based degree and then specialize in my field of interest in grad school. So I read up about chemical engineering and I think it would be an interesting major, but my real interest probably lies in biotech.Is it possible to transition form chemical engineering to bio-related fields in grad school?

This will probably to a high degree depend on the (exact) curriculum and prerequisites of your chosen bachelor and master.
Also note that I'm not from the US and judging from the terms you are using, it seems that you are, so everything I say is also a bit speculative.
In general biochemistry and to some degrees also biotechnology will have a lot of overlap with many aspects of chemistry (or at least organic chemistry). Depending of the focus of each program this might, make it possible to switch over from one to the other. One thing you will definitely not learn in any chemical mayor is molecular biology, which may well be a requirement for studying in any biotech related field later on.
If both your majors focus more on the technological aspect and less on the biological or chemical you should probably be fine. The equipments used in (modern) biology and chemistry is in many cases similar, though biotech involves more equipment specialised for the handling and analysis of cells. The underlying principles are still the same though.
In your case I would recommend you to check the requirements of different MS or grad schools, that you'd be interested in first, and the see if you can meet these with a chemical engineering mayor (and maybe/probably some added courses like molecular biology).

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Why doesn't nitrogen diffuse into blood?
In school, I have learnt that the deoxygenated blood brought in to the Alveoli by Pulmonary Arteries contains Carbon Dioxide. And that Carbon Dioxide present in the blood diffuses into the Alveoli and squeezed out with the help of Diaphragm.
Then, why doesn't the Nitrogen present in the Alveoli gets diffused to the blood? My guess was that the blood vessels don't allow anything other than CO2 and O2 to pass through.
But I recently saw a video on KhanAcademy where Sal said that some amount of Nitrogen does get mixed with blood. Is Sal right? If yes, then why doesn't the whole Nitrogen present in the Alveoli gets diffused from there (where it is present in high concentration) to blood (where it is present in low concentration)?
To summarize,

Why doesn't the inhaled-Nitrogen present in the Alveoli diffuses into the blood present in Pulmonary Veins, similar to how CO2 present in blood gets diffused out to the Alveoli?

It does get diffused, your blood has plenty of N2. Actually, the arterial pN2 is higher than the pO2, making N2 the most abundant gas in your blood.

@GerardoFurtado So, Sal Khan was wrong. I guess you should put that as an answer so that I can accept it.

He's technically correct, if he said "some" amount.

@GerardoFurtado How? Why only some?

Because technically some is indefinite, it can be anything from a very little amount to almost 100%. Well, I was about to post, but someone already did it.

@GerardoFurtado Okay. Thank you for your help! :)

Can you please link the video? I want to check what he says exactly (he may be wrong, after all).

(Alas, GerardoFurtado was never provided the link, and now his account is deleted too. Sorry, Gerardo, I didn't see your comment earlier :-P)

I like it that nitrogen came to your mind ;)
I guess in school they didn't tell you about the nitrogen at all, for the matter of simplification, because it is of no function in the body and the $O_{2}$ and $CO_{2}$ are the important gasses for biological function of breathing.
However, all of these small gas molecules are very small and generally the biological membrane is very permeable to them. That's why the cell cannot decide to let $O_{2}$ and $CO_{2}$ in and $N_{2}$ not as you suggest.
(However, the cell is able to control the permeability of these gases to some content, based on the level of cholesterol in its membrane$^1$)
The process of gas exchange is generally passive. In alveolar membrane the gas flows from the site of its higher concentration (in case of gases we talk rather about partial pressure) to the site of lower concentration. The speed of this process depends mostly on the difference in partial pressures and if you let the blood "interact" with the air in alveoles for long enough, partial pressure of all small gas molecules would come almost to equilibrium. (This happens under physiological conditions for all of the three mentioned gases)
Khan academy is right too actually. This is because as $N_{2}$ isn't either produced or consumed in the body, its partial pressure in the venous blood is similar to that in the alveolar air, and there is no force to cause its movement between these two compartments in general.

In the table you can see, that the partial pressure of nitrogen in the blood is the same as in the alveolar gas.
Picture source

"the gas flows from the site of its lower concentration to the site of higher concentration" This is physically impossible.

@GerardoFurtado thanks, random mistake. corrected

Nitrogen is not a metabolic gas, its partial pressure is very high. No compound of blood can react with Nitrogen hence its diffusion is not possible.
its diffusion is only possible when a person is suddenly lifted from depth of ocean, such diffusion causes bubbles in blood vessels leading to death due to disease called KESHAN
THIS IS WHY WARNINGS ARE GIVEN PRIOR TO SCUBE DIVING

Please add some references explaining how you got this answer

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What is this pollinator's name?
What is the name of this bee pollinating a lemon tree?
Area: south-central Europe

I'm not an entomologist, but it seems to me that this bee is a Xylocopa, or a carpenter Bee:

Xylocopa iris
If this is, in fact, a Xylocopa, narrowing it down to the species level will be very difficult, since the Genus has more than 500 species. You could start with one of the most common carpenter bees in Europe, Xylocopa violacea:

Xylocopa violacea
However, I believe that this may be in fact Xylocopa violacea because of the antennae: you can see a little orange stripe next to the tip of the antenna in the bee of your photo, just like in the bee of the photo above.

Besides the orange stripe, the "hairyness" of the bee seems more similar in the second photo than in the first one. And the front wings look brown, like in the second photo.

@bli Indeed. The first photo is just a photo of any bee from the Genus Xylocopa. Later, when I found Xylocopa violacea, I edited the question but I kept the first photo.


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How to identify a coiled coil from the amino acid sequence?
I was wondering, when we have an amino acid sequence, is it enough to check whether the positions a-d correspond to hydrophobic amino acids in order to say whether it can form a coiled coil structure? Or would we need to make sure the other positions are not hydrophobic too?
All help greatly appreciated.

The heptad repeat, denoted [abcdefg]n, typically has hydrophobic residues at a and d, and polar/charged residues at e and g.

From here.
There is a prediction tool with useful images here.


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What are the microscopic mechanisms of plant branching?
For a long time I've been idly interested in how the shape of a complex organism gets determined during development at a microscopic level. Recently I've realized that plants could be a good place to start trying to understand that, because the structure of even a quite complex-looking plant can sometimes be described by a few simple behaviors. Here are some examples.

My radish plants have a single base where all foliage grows from. After it's first two seed leaves, it grows some number of large rough leaves which all descend to the same point. No other branching ever takes place.
My pea plants have only one long stalk, which grows symmetrical pairs of leaves at regular intervals. Occasionally, the base of a leaf pair spawns a mini-stalk, never more than 3 or 4 leaf-pairs long, ending in a "claw" of three tendrils. Most of the time, one of the three tendrils will split again in three (always the one aligned with the "top" of the stem, as determined by leaf orientation)  .
My fennel plant has thick bases to its stems which each extend a few inches before branching starts. At that point, it branches at regular intervals in symmetric pairs of fronds, which in branch the same way. Those third-layer fronds branch at regular intervals but alternate sides, and there are always exactly four layers of branching no more and no less.
My basil plants seem roughly able to grow branches in any advantageous spot, with no rigid rules or geometric behaviors like the other examples.

My background is in mathematics, and all my knowledge of biology is dated to high school. I've always been confused by how DNA is presented as a "list of proteins", when it is clearly so dynamical and not static: each cell type only produces some of those proteins, and those proteins can in turn determine what proteins it's children produce, I guess, and this can create a rich (non-linear) hierarchy of tissue differentiation out of a linear list.
For a really complex organism like a mammal I guess that our understanding of how DNA gets actualized is phenomenological (i.e. we can tell that gene X correlates with macroscopic trait Y, even if we have no idea what the signalling mechanisms are behind it and which cell types produce a relevant protein and when.)
But is this true also for plants, or do we have a deeper understanding of what proteins differentiate, for instance, the four stalk types of a fennel plant, and why each type can only produce the next one? I think simple animals like sponges and nematodes and cnidaria probably would be as helpful as (or more than) plants, but as a gardener I see these plant geometries every day and am fascinated by them.
Does anyone know of a good reference, book or online, that discusses these topics? I'm okay with something a little out of my technical depth - I'd prefer a difficult answer to an incomplete one.
EDIT: Leaf architecture is also interesting, and probably inseparable from branch architecture on some level, but I focused on stalks and branches probably because I don't have the terminology to meaningfully describe leaf architectures.

It sounds like you are asking for an explanation of how genetic regulation works, which may be too long for the site. for just branching this will help https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1630745/ for gene regulation try this https://ghr.nlm.nih.gov/primer/howgeneswork/geneonoff

Oh this video is a good starting point as well https://www.youtube.com/watch?v=3S3ZOmleAj0 Hint we actually know how many gene lead to macroscopic features. You should also be looking for embryonic development as well.

Thanks a lot John! That video was a really great foundation, but it doesn't go into how/why gene regulation would change in a cell line, which I think is more what I'm interested in. I'm really looking forward to looking at that first paper, and then once I have some context, diving into the second one.

It doesn't change in a cell line, which ones are switched on or off change. There are dozens of reasons this can occur, cells signaling each other, Internal cell pathways,  external environmental factors, ect. https://en.wikipedia.org/wiki/Cell_fate_determination

By the way, this was a refernence request and not a request for a direct answer, so if you want to repost that as an answer it will be accepted!

I may have used the wrong terms, but I think we're saying the same things. In the fennel plant, for instance, cells in a layer-one frond at some point start giving rise to cells that form a branch, which have somewhat different gene expressions, right? Cell line may not have been the right term. (There are also other reasons gene expressions change, like the presence of lactose in the video, but this one narrow mechanism or pile of mechanisms is what I'm most interested in)

I'm not being vague on purpose but there are literally dozens to hundreds of signalling pathways involved in branching across all plants.

And of course even in the branching case, I suppose those other mechanism must be at play, since nutrition and weather surely affect how and where a plant branches, and this paper points out that long-distance signalling does as well. So I'm maybe I'm mistaken to differentiate between them.


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What is the name of this plant I found in ROAD HIGHWAY?
Location of the plant is South India,
Plant stem looks like Banana.

Down vote, why so?

@AScientist thank you for detailed suggestion, can you give me advise where else I can post this pic to get its ID.

I don't know if any botanist can identify it with only this image. I think you should see this to write a standard identification question. https://biology.stackexchange.com/questions/59005/streamside-plant-identification-oregon

I don't know why @DhanrajKumar your post got down vote. he provided nice quality picture & also I know the answer to your post.

It is Fishtail Palm, Example picture look like this:


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What does factor VIII have to do with thromboplastin formation?
I've got the following question and I'm afraid that the question doesn't match with the answer...
Factor III (rather than factor VIII) is known as thromboplastin or tissue factor and it makes sense that the factor III deficiency is related to thromboplastin formation. Isn't it?
What does factor VIII have to do with thromboplastin formation?

The question refers to factor VIII, not factor XIII.

Typo. My mistake. Thank you for the attention.

You have 3 more typos: there is an o in thromboplastin.

Have you done any research, for example, looked at Wikipedia for the function of Factor VIII? If so, please explain in more detail why you're still confused. Thanks.

OP is still confused because the question he/she is quoting has a wrong answer. The correct answer is C.

@GerardoFurtado thank you for the attention, it was corrected. I'm a non-native English speaker and it may happen, I'm sorry for that.

@anongoodnurse Regarding to research, I did a lot, and also discussed with my friends on Whats-app group, I came here as a last resort. We have a confusion about this question. I'm confused because the factor III by itself is thromboplastin and since it's absent, then we don't need to talk about absence of factor VIII which interrupt thromboplastin formation (and by the way it is by itself not so clear, because factor III takes place before factor XIII works), I hope I explained myself well.

I am so confused... Why are you referring to FIII? The question is about FVIII (deficient/defective in hemophiliacs and patients with Von Willebrand syndrome.)

Indeed I referred to it as well, but just as possibility of a typo in the original question (FVIII instead of FIII). One of my thought was that FIII by itself is the problem of thromboplastin formation because FIII is thromboplastin. But as I said I don't reject the possibility that the question is about FVIII and I just don't know why the official answer is thromboplastin formation in this case.

As far as I can see from OMIM https://omim.org/entry/134390 there are no hereditary conditions associated with FIII deficiency so I think it unlikely that it is a VIII/III typo. I agree with @GerardoFurtado, if the asterisk is indicative of the 'correct' answer then this is a mistake in the question (or actually in the answer to the question).

Thank you for the additional information. One of my classmate claims that  Thromboplastin is involved in the conversion of prothrombin to thrombin and therefore the answer is thromboplastin ("it needs factor xa to do the conversion but it needs need also factor VIIIa to aid in the conversion"). Honestly, I still don't understand.

@UbiquitousStudent Is the formation of thromboplastin a step in blood coagulation?

"Thromboplastin (TPL) is a plasma protein aiding blood coagulation through catalyzing the conversion of prothrombin to thrombin." (wiki)

@UbiquitousStudent Okay. So if the answer is C, what is the question?


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How does Reissner's membrane rupture cause Ménière's disease symptoms?
In Ménière's disease, an ednolymphatic hydrops (EH) in scala media leads to a distention and, eventually, rupture of Reissner's membrane. This results in an influx of K+-rich endolymph into the Na+-rich perilymph of scala vestibuli.
Supposedly, this causes an "injury to the sensory and neural elements of the inner ear, which manifests clinically as sudden hearing loss, tinnitus, and vertigo."
What is the pathophysiological mechanism? Aren't these elements part of the Organ of Corti, not in the perilymphatic space?

It would be nice if you could cite your sources for most of your information. This appeals to the community that you have done your research.

source: my ENT textbook and BMJ

It would be better to mention it in your question itself with links that can guide the community to the sources so they can read more if needed. See Here on how to link your sources.


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Shouldn't recording electrode have as low resistance as possible?
Following quote is from this wikipedia page on single unit recording.

Intracellular single unit recordings require electrodes be inserted through the cell membrane to record from within the cell. Glass micropipettes or metal electrodes may be used for intracellular single unit recordings, but glass micropipettes are preferred because their high input resistance allows more precise recordings for measurement of resting potentials.

How high input resistance helps better recordings? Shouldn't recording electrode have as low resistance as possible?

Can you please offer your proposal for the situation? Do you know which variables are relevant there? What is your measurement setting?

Could it be that you mean impedance instead of resistance? It is one of the electrical properties that is the least understood by biologists (like me) and in the biological community there are lots of myths and rumors about whether impedance should be high or low. This might help: https://electronics.stackexchange.com/questions/21787/why-is-high-input-impedance-good or this: https://www.quora.com/What-is-the-influence-of-electrode-impedance-on-EEG-data-recording (though it refers to EEG)

For accurate measurement of the membrane potential, it is crucial to have as little current flow through the measurement device as possible. Otherwise, the equilibrium of leak channels that generates the resting potential would be disturbed. See diagram and text from Axon Guide 3rd edition below:


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How it is determined that a particular gene or set of genes is responsible for a trait?
How it is determined that a particular gene or set of genes is responsible for a trait? Is it just a statistical analysis of people showing and not showing the trait and the genes they have (or don't have) and their variants (alleles)? Or, there is something more.

The classic procedure was to establish an association, typically by observation, statistics, or reasoning. Then, you start doing the molecular genetics. First, knock out the gene(s) and observe the phenotypic effect. Second, express the gene(s) in a mutant knockout organism and see if the phenotype come back. Attaching the gene to an inducible promoter makes this pretty simple to do. However, this basic procedure has had to get much more complicated and nuanced over the years, as we've expanded the repertoire of genes that we want to study.

This "knock out the gene(s) and observe the phenotypic effect" is for animals right?

@AmitMaurya You can knock-out gene to any living creature; procaryote or eukaryote (incl. plants, fungi, animals, and others) and even viruses. The only theoretical restriction has to do with ethics. It is typically not allowed to make such experience on humans.

Yes, I was refering to ethical considerations.

Then how mechanism is established in humans?

In the below list of technics, I am assuming we are talking about haploid individuals (to avoid discussion about dominance relationship) and assuming no epistasis but the technics can 'easily' be extended to include these cases. I also assume we are talking about coding regions.
Note that I am more of a biostatistician / population geneticist than a molecular geneticist, so I am pretty sure I will unwillingly bias my list toward what I know most. There is a lot to say about every single technic but of course, this cannot be covered in a single StackExchange post.
Technics

Statistical association (observational study) with existing variance in natural population. Do carrier of a given allele have another trait value than the carrier of the other allele. Possible confounding variables include population structure and linkage disequilibrium.

Population structure: To deal with this confounding variable, we can make a genetic PCA and include the first two axes as covariate in a type I sum of squares regression. We can also use tools such as STRUCTURE to infer the population structure and then use the inferred groups as a nominal covariate.
Linkage disequilibrium: We typically consider a number of marker that we try to associate to a specific phenotypic trait. It is impossible to tell whether the observed association is directly caused by the marker we observe or by a tightly linked marker. For further investigations below technics must be considered.

Statistical association (experimental study). It is possible to create the treatment groups by knocking out (or other technics such as the now popular CRISPR technic) specific gene in out in some individuals and look for a statistical association. The advantage of such manipulation is that we can create the optimal level of genetic variance we need to increase our statistical power.
Transcriptome analysis. Making sure the coding region is being expressed in the tissue of interest. E.g. if you expect a given gene to affect myosin tertiary structure, you might want to make sure the coding region is indeed expressed in the muscles and not only in the brain!
Protein action. It is also possible to study the specific action of the protein coded by the coding region of interest. Such studies typically require the study of an entire biological pathway and is often demanding and quite expensive. Here the methodology are diverse but they're discussion is both outside the scope of the question and outside the scope of my knowledge.

Example - Genetic Basis of Color Adaptation in mice
In a comment, you asked

Is there any research paper, review paper or blog which covers entire details how the association and mechanism was established for any of those discoveries?

In most study cases, not all of the above steps are being considered. Also, even if it is the case, such study will be covered by several peer-reviewed papers and not a single one. I don't know of any peer-review paper that explains the whole process for a particular case but those probably exist.
There are documents that explain such process for layman. For example From Darwin to DNA: The Genetic Basis of Color Adaptations by Hoekstra is a standard reading for undergraduate that will interest you. It is easy and pleasant to read. Quoting from this article

In this essay, we will take a journey — into the laboratory and the field — to understand the genetic basis of adaptation in natural populations of mice, and the phenotype we will focus on is the color of their fur.

The gene of interest in this paper is melanocortin-1 receptor (Mc1r). Depending on what level of understanding you want to reach, the article might be a bit too introductory but it refers to some good peer review papers that will allow you to further your knowledge.

First two methods establish the association, and fourth one establish the mechanism. Is that correct inference?

Yes. First two are pure staitstial association. 3 ensures that the association seems to make sense. 4 goes into the detail mechanism of why such association exists

There must be traits controlled by a single gene. Is there any research paper, review paper or blog which covers entire details how the association and mechanism was established for any of those  discoveries?

@AmitMaurya See edit! I hope that helps

I think WCGNA is a fascinating method of unsupervised gene-trait relationship determination, and they have very nice tutorials on how one might carry out such an analysis (ref). The only issue with unsupervised methods, of course, is we often use them when we have no other information about a system but they're also prone to inaccuracies. A good starting point, however.


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what are the ethical considerations when preparing a bacterial culture for testing antibiotic resistance?
I cannot think of any ethical issues associated with preparing a bacterial culture to test antibiotic resistance. The bacteria I am using is Bacillus Megaterium so its not pathogenic.
Thanks in advance for your help!

I'm voting to close this question as off-topic because ethics (incl. ethics in biology) is a field of philosophy, not biology. You should give it a try on Philosophy.SE.

While I think the question is off-topic, I could not help but trying to answer it! It is easy to find ethical issues in every activity.
Potential ethical issues

You are killing bacteria
Your research has an environmental cost. You consume loads of plastic thingies for example.
Your research costs money as well. You consume tax payer money (depending on your source of funds)
You are selecting for anti-biotic resistance and might, by mistake, release them in nature (of even they are not pathogens, they might become, they might transfer their resistance to pathogenic bacteria as well or your experience may have all sorts of unexpected consequences)
Are you sure it is not pathogenic? We are never sure of anything, so just don't take risks.
Don't play with nature, you are not God!
Are you helping those nasty big pharmaceutical companies, huh?
You are a clever person. There are so many other things you could do for the world that would be so much more beneficial. Your time could be used for better purposes. You could work on improving sanitation conditions in India, or improve women's right around the world, or help children involved in the current civil war in Somalia for examples.

Basics of philosophy of ethics
For any question of ethics, one has to define his/her own values and from this point this person can formulate an opinion on a particular case. Of course, I personally do not feel bad about killing bacteria and consider antibiotic resistance a very important field of study to improve our everyday well-being but other people may disagree based on their own values.
I am not formally trained as a philosopher. So, please read the wikipedia articles on ethics and values I linked above and if you have any other question of Philosophy, you can ask them on Philosophy.SE

You don't think studying antibiotic resistance is a pressing concern, or is less worthy than the other pursuits you listed?

I did not express my personal opinion. I just listed possible ethical issues. It is up to someone's values to define what is ethical or not. I feel perfectly fine with killing bacteria for example. And of course, I consider antibiotic resistance a very important field of study that has high impact on our everyday well being.

Fair enough....

@canadianer I have now edited the post to try to clarify that I am not expressing my personal opinion. Thanks


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1mm-long insect ID from Tennessee
I live in east Tennessee. I went outside today (May 27.2017) and saw all these tiny insects all over my truck.
They are yellowish in color and have 6 legs, one solid body (including head). They move pretty quickly (like a chigger)
What are they?

East TN you said. Does TN stands for Tenessee or Tunisia (both being typically abbreviated TN)?

Very important to mention that they are six-legged.

@adjan and I are being a bit mocking today! Sorry about that. I edited the post assuming that you live in Tunisia (given your user name and given that a Tunisian would probably name the country fully by fear people would not understand). I  also removed the (quasi-) tautology (6-legged insect). +1

@Remi.b "I edited the post assuming that you live in Tunisia." "I live in east Tennessee." ;)

That was a typo.

Welcome to SE Biology. I know that computer graphics are difficult, but the photos you have posted do not display in my browser because they are about 10 times larger than necessary and do not show enough detail. I have processed the first for you, but if you need to post again, do an internet search to find out how to downsize photos.

The only reason I uploaded the large photos is so that you could zoom in and see the insects better, (The better to see you with my dear ((Wolf))

Thanks for all the comments, yes, east tennessee

I thought it might have been a Thrip, wasnt sure about that

Include the size (approx is ok) in question. maybe 1mm or half-mm? Best if include the size (height or width) of reference,  "SRF" logo, which is easily measurable.

The insects you have found must be of a species of thrips. This excerpt from Wikipedia fits your description well:

Thrips (order Thysanoptera) are minute (1 mm long or less), slender insects with fringed wings and unique asymmetrical mouthparts. Different thrips species feed, mostly on plants although a few are predators, by puncturing and sucking up the contents. Approximately 6,000 species have been described.

I won't try to identify the exact species, but here is a photo of a yellowish-orange thrip I have found:

Image source:
https://6legs2many.files.wordpress.com/2012/04/thysanoptera_thrips_fringe_wings.jpg


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Energy efficiency of muscles and animals as a whole
When human or animal do some work, they use energy from their food. What is known about overall efficiency of this process?
Say a horse is turning a winch and does 10,000 kJ of work. How much more food will it eat to sustain that effort (compared to when it just stands around)?


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Isn't heritability more important to genic capture than just genetic variance?
Rowe & Houle (1996) give two criteria for the selection of costly female choice:

Condition dependence of sexually selected traits
High genetic variance in condition

Regarding heritability, they wrote,

comparisons based on heritability are misleading, as Fisher's fundamental theorem of natural selection shows that the response of fitness to selection depends only on the additive genetic variance, and not on other components of variance.

However, the magnitude of environmental variance should matter for the selection of female choice for sexually selected traits, since the more environmental variance means the less likely offspring of fitter males will be fitter themselves and the less likely females should be to incur costs to mate with fitter males.  Am I not correct?  Is this an oversight on their part?

I would suppose they talked about genetic variance for fitness while you are expecting them to refer to genetic variance for female choice. Fisher's fundamental Theorem stands right when talking about the genetic variance for fitness, not for another phenotypic trait such as female choice. Do you think you were mislead by this confusion? Note: I have not read the paper.

Their paper is intended to explain the evolution of female choice.

Possibly relevant: the breeder's equation can be written in two different ways. for a given selection differential (covariance of trait with fitness), response to selection is proportional to heritability. But for a given selection gradient (regression of trait with fitness - i.e. the covariance divided by the total trait variance), response to selection is proportional to additive genetic variance. Between the two versions, you're just shunting the V(P) denominator between the two right hand quantities. See https://biology.stackexchange.com/a/52250/26665

Since the regression of fitness with itself is just 1, the response to selection of fitness is proportional to additive genetic variance (that's kind of like a discrete version of Fisher's Fundamental Theorem)

But ya I see your point - if e.g. horn length is condition dependent, but condition has high environmental variance, then shouldn't horn length be less correlated with fit genes? So shouldn't the same amount of "horn-length preference", get you a smaller fitness benefit for your children?

Like you're right, females aren't directly selecting for fit genes, they're selecting for a fit phenotype which may be strongly or weakly correlated with fit genes

Thank you, sir.  These comments are helpful.  They seem to be equating the benefit a female receives from choice with response of fitness to selection, which I do not understand.

@David Bahry, I appreciate your time.  That was very helpful.


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Mackerel evolutionary health affected by loss of predators?
I notice that Atlantic Mackerel (Scombrus scombrus) is endemically affected by parasites. In one study I read that the researchers found that over 70% of the mackerel sampled were infected with parasites.
Is there any evidence that the diseased state of the mackerel population is possibly due to loss of natural predation? The major predators of mackerel are tuna and cod, both heavily fished by humans. At one point cod was fished nearly to extinction and is still considered endangered. Since cod will typically catch the laggards and least fit of their prey fish, like mackerel, I would expect that over time this predation would tend to eliminate sick or unfit fish. Without this natural predator, perhaps it is leading to sickly conditions in mackerel?
Is there any basis for this thinking?

A few comments: 1) For thinking about whether your hypothesis is plausible, it would be handy to know how these parasites transmit (but it is likely there are several parasites and the mode of transmission varies from parasite to parasite). 2) Can you please link to the study you refer to? 3) Do you have any reason for thinking that the rate of parasitized individuals has changed over the period of over fishing? 4) I think (but might be wrong) that warm waters often tends to increase parasitism and climate change might be a potential cause as well.


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Co dominance, breeding and genes
Let's say we are talking about a complex being with many variations.
Let's take coat colour as an example and pretend we have a creature with codominant genes to do with coat colour (for example BR (B for black and R for red, assuming they're both dominant and visible).
We now breed said animal to a co dominant coat type of a different variation (for example, YW (Y for yellow and W for white, assuming again that they're both dominant).
Assuming all 4 dominant genes are as dominant as each other (so red isn't going to appear over yellow, for example)
What comes out of said breeding?

I believe you are mistaking co-dominance with semi-dominance. What is the color of BR individuals? Do they have red and black hairs?

The animal will have both colours present and visible in its coat. If it helps, we can assume the parents had the genes Bg (black (dominant) and green (recessive)) and and Rp (red dominant and purple recessive)  the 25% would have been BR which is what we got

Well, I just posted an answer but now you're talking about recessive alleles, which render my answer useless. I just deleted it.

Well, assuming we have 2 parents with the genes Bg and Rp, there is a 25% chance of an offspring with the gene BR. folkweing the same pattern we have another of the same species with the genes YW. If we bred those two, what happens? If all 4 genes are dominant, do they separate to create a new variation (such as the chance of BY) or do they mutate to create a whole new type of colour (perhaps YWRb (yellow white and red, with the black carried as recessive?)

Reading your comments I strongly suggest you study monofactorial inheritance first, and then ask your question here. Don't get me wrong, but there are a lot of things in your comment that make no sense and show us that you have a wrong concept of genetics.

I am not sure I understood your question. I will try to rewrite your question below with my own words and you will let me know if I udnerstood your question correctly.
Description of the genetic of interest
There is only one locus for coat color. Individuals are diploid. At this locus, there exists 4 alleles in the population. B, R, Y and W. BR individuals are both black and red (as B and R are codominant). Another individual is YW and its phenotype is yellow and white (as W and Y are codominant)
Question
What phenotype do BY, BW, RY and RW have?
Answer
There is no way to know! Relationships between alleles, say Y and B in determining a given phenotype cannot be extrapolated from relationship B and Y have with other alleles. A relationship between two alleles in determining a phenotype is specific to a pair of alleles.
It is for example theoretically possible that A is dominant over B and B is dominant over C and C is dominant over A.
In your case, as you only have codominant relationship, it is tempting to expect that BY would be both black and yellow but there is really no way to be sure of that from the "Description of the genetic of interest"
EDIT
You have now changed your post. I don't really understand the new question either. You seem to imply that two alleles may be both dominant. This is impossible. They can be co-dominant.
I think your issue is that you are trying to associate a property of relationship between alleles as a property of an allele itself. Keep in mind, that saying that an allele is dominant only makes sense in a particular context that is in relationship to another allele who will therefore necessarily be recessive.

Could the crossossing of all those dominant genes create a mutation? (Or make a mutation more Likely?) also even if we get let's say a RW (red and white), is it possible for the other genes to have been carried over still and be present in said offspring?

It does not mean anything to say that a gene is dominant. An allele can be called dominant when considered in its relationship to another allele at the same locus. Relationship between allele have no causal effect on mutation production so I don't understand why you ask if it would "create a mutation".  Specific alleles may affect the mutation rate though but I don't think this is where you are trying to go.

I do apologise if I don't make much sense, I'm really struggling to understand co dominance and how it affects breeding and mutations into new variations. To put it more into a sort of context we can look at horses. There's a colour called piabald (black and white patches on black skin). Did that colour originate from a BW (black white co dominant) and mutate into one gene (call it P for dominant piabald, which can now be carried with any other recessive (such as b for buckskin (a recessive colour))

No worries. I know what it is to enter into a new subject. It can be very challenging to ask clear questions. I don't really understand your question again and don't really understand what's unclear to you. You might want to review the definitions of mutation, gene, allele and locus.


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Internal organs temperature
We know body surface temperature rises during fevers. Do the internal organs' temperature also rise during fevers? How do they (internal organs) maintain their temperature? Will there be a variance of temperature among them?


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Is it possible to obtain single strands of DNA in solution?
Being that it is relatively simple to extract DNA from a variety of sources, what further technique can be used to separate the two complementary strands in solution?

Heating the solution? I doubt if you know about PCR...

There is usually a denaturation step in a typical PCR protocol, see e.g. here, which serves exactly this purpose: the strands are thermally divided (typically at 95 °C for a few seconds). As you can see, this is a very common process, but the strands only remain denatured if kept at high temperatures.
Room-temperature strand separation in regular buffer solutions will be very hard, because annealing (the opposite process, where two complementary strands pair up) is thermodynamically favourable.
More permanent separation might be obtained by dissolving DNA in particular solutions, as described here, where DMSO seems particularly effective.
This results in separated strands at room temperature, but both strands will clearly still be present. One might think about separating the two with various methods (e.g. HPLC), but I doubt these solutions are compatible with regular HPLC columns.

Are there nucleases that could recognize a sequence on the unwanted strand and cut it? That turn the long unwanted strand into 2 shorter strands. You could then separate them from the long desired strand by electrophoresis.

definitely yes! you can check here for a list of nucleases that cleave single stranded substrates. I think the problem would then be that even the shorter fragments (at least one if not both) would re-anneal...

I've added this answer because the comment on the accepted answer suggests that they are interested in isolating separated strands of a dsDNA.
Single stranded DNAs can be separated by polyacrylamide gel electrophoresis of denatured dsDNA.
End-labelling of dsDNA followed by strand separation was a key technique when sequencing DNA by the Maxam-Gilbert method (chemical sequencing). The figure below is taken from this paper.

For this experiment dsDNA fragments were end-labelled (radioactive label) then the strands were separated by heating to 65 °C in 10M urea. The sample was cooled rapidly and then loaded on to a polyacrylamide gel. (Because the two strands of dsDNA will usually have different base compositions they will be resolved during electrophoresis.) The DNA bands were then visualised by autoradiography. As explained in the paper the absence of a second band for the 165 bp fragment is an artefact of the labelling method (i.e. one strand was unlabelled and the visible band was ssDNA.). As you can see, except for the smallest fragment, individual strands were resolved by this method. Once separated these ssDNAs can be isolated from the gel slices.
However, I don't think this method would be useful for large DNAs because the gel wouldn't resolve them well enough.


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How does DNA from sperm fuse with DNA in egg?
I see this statement all the time "half of our DNA (23 chromosomes) are from mom and 23 are from dad". Fine, but which chromosomes in our nucleus are from each parent? When I think of nucleus (before interphase), I imagine a total of 23 unique chromosomes and 23 copies of them. In the first cell after reproduction (zygote), does chromosome 1 from mom align with chromosome 1 from dad? When zygote divides (after S phase) do you now have 4 copies of the same cell? Since choromosome 1 from mom and dad is the same.
What role does crossing over play in all of this.
I have done lots of reading but nothing is helping me connect the dots.

By "23 copies of them" I mean the "copies" that we receive from one of the parent. So in our nucleus, we have our whole genome X 2 (except Y chromosome, which is only once).

First, to clarify on the number issue and parental origin of the chromosomes. For the moment, disregard crossing over. Then, you would begin with an adult somatic cell in the growth phase, having 46 chromosomes, two of each kind, that is, 23 pairs (assuming sex chromosomes to be of the same kind, including the case in males). Then, in the S phase, each chromosome replicates, creating exactly similar sister chromatids, each of these sisters being similar to the single chromosome the cell had in growth phase. Each of these chromosomes with two chromatids, sends one to each daughter cell, making the daughter cell exactly like their parents. In meiosis, after this step, one of each kind of chromosome separates into a gamete, so that instead of 23 pairs, each gamete has only 23 chromosomes, one of each kind. On fusion of two gametes, you would have the original configuration again.

Crossing over, just means that when the two chromosomes of a particular kind separate during meiosis, they exchange corresponding material. If no crossing over happened, the gamete would either have one of the two same-kind chromosome, or the other. But due to crossing over, you create a different set of genes on these two chromosomes, different from the ones fond elsewhere in your body. So if say two chromosomes of the same kind have genes $ABC$ and $DEF$, if no crossing over happened, the gamete would have either $ABC$ or $DEF$. But crossing over makes possible combinations like $AEF$, or $DEC$ etc.


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Which nucleotide as start point for maximum parsimony?
Background
Maximum parsimony is used to build an evolutionary tree by choosing the "simplest" one. I see a lot of examples about how this should be done. For example:

Question
However it's not clear for me WHICH nucleotide should be used as starting point?
Let's consider the first tree(from the figure above):

Nucleotide G was chosen as starting point resulting in one mutation, however if we choose T we would have two mutations and if we choose A we would have three. So what determines the nucleotide which should be used to start with?

Both the text on your diagram and the WP link explain this don't they? The chosen ancestral residue is the one which, in order to fit the tree, needs the fewest total changes. If this doesn't answer your question then maybe you need to rephrase it.

For every tree the number of mutation should be counted to determine the simplest tree rigth? So let's say we have 4 sequences --> 3 unrooted trees --> write every tree down --> for every (informative) position fill in the nucleotides and count the number of mutation needed. But to count them you need to know the "ancesteral nucleotide". So as you suggest you should make the trees as simple as possible (by selecting the best fitting nucleotide as ancestor) and than from these trees againg select the simplest one (the one with the fewest mutations)?@AlanBoyd

Yes, so you need to try the tree with each possible ancestral nucleotide in order to find which gives maximum parsimony (lowest number of substitutions).

Hmm so actually you can make 3x4 trees in the case of 4 sequences? and than select the simplest? @AlanBoyd

The "starting point", or ancestral state, is chosen so as to obtain the most parsimonious tree.
Parsimony is used both for choosing the topology and for choosing the ancestral states for a given topology:
1) The parsimony score for a given topology is computed for the set of ancestral states minimizing the number of transformations.
2) Then, the topology minimizing this minimized number of transformations is chosen as the most parsimonious tree.

Do you have any references for that? I would like to read more about this @bli

@RickBeeloo In terms of algorithms, the process may not necessarily be implemented the way I describe it, but by definition, the most parsimonious tree needs to have its internal nodes states optimized for minimizing the number of transformations, otherwise, we might end up with the wrong topology.

See for instance definition 11.18.1 in https://ab.inf.uni-tuebingen.de/teaching/ws06/albi1/script/phylogeny_31Jan2007.pdf: "where the minimum is taken over all possible labelings λ of the internal nodes of T"


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Can neutrophils kill bacteria inside other cells?
Are neutrophils able to get inside epithelial cells in order to kill bacteria. Therefore, even if a bacteria gets inside the epithelial cells can the neutrophils get inside the epithelium to kill the bacteria?
Also when the bacteria get into blood stream can neutrophils kill the bacteria?
I am not from a biology background. So, a simple explanation will be helpful

Please do some basic reading on neutrophils (or whatever your topic is) before you post a question. We want to help clear up confusion or solve problems in people with a sincere interest in Biology. But we do ask for evidence (in the question) of what you read about it. Thanks.

Are neutrophils able to get inside epithelial cells in order to kill bacteria.
  Therefore, even if a bacteria gets inside the epithelial cells can the neutrophils get inside the epithelium to kill the bacteria?

No. Firstly because bacteria (except for very special cases) do not enter epithelial(or other) cells - that's what viruses do. Second, neutrophils recognise bacteria based on markers on their cell wall. These markers can come from the bacteria themselves, or from the innate immune system (see complement system) that 'marks' the bacteria, in any case being inside another cell would protect bacteria from neutrophils. Cases are like these are handled by the CD8+ T-cells of the adaptive immune system.

Also when the bacteria get into blood stream can neutrophils kill the bacteria?

Yes, that's their job and neutrophils are usually inside of the blood(stream), so they could find and kill bacteria there.


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Do birds ever fly in clouds?
Do (some) birds ever fly in fog or clouds so that they would not be able to see either the ground or the sun? Assuming the visibility is good enough so they can see obstacles in time to avoid them.
If they do, how do they maintain straight flight?
Inner ear is inadequate in the air, because it can only sense the sum of gravity and acceleration, which is just the (reaction to) aerodynamic forces and those are always orthogonal to the wings. To an extent, it can also detect rotation, but this is not good enough to keep precision for minutes and hours in cloud. So how do birds know where is up?

Yes, they do.
Pilots normally say that "birds are day VFR only", you're gonna read this a lot on the internet. VFR means Visual Flight Rules, where the pilot operates the aircraft in weather conditions clear enough to allow the pilot to see where the aircraft is going. Thus, they are implying that birds avoid flying at night and inside clouds.
However, this is wrong. Birds do fly inside clouds (and at night), especially migratory birds that have to fly non-stop for weeks or months. They cannot avoid flying at night (of course) and, in several situations, they cannot avoid flying towards a cloud.
According this paper in Science, from Weimerskirch et al. (2016), frigatebirds can even do this on purpose!

We studied the three-dimensional movements and energetics of great frigate birds (Fregata minor) and showed that they can stay aloft for months during transoceanic flights. To do this, birds track the edge of the doldrums to take advantage of favorable winds and strong convection. Locally, they use a roller-coaster flight, relying on thermals and wind to soar within a 50- to 600-meter altitude band under cumulus clouds and then glide over kilometers at low energy costs. To deal with the local scarcity of clouds and gain longer gliding distances, birds regularly soar inside cumulus clouds to use their strong updraft, and they can reach altitudes of 4000 meters, where freezing conditions occur. (emphasis mine)

Source: Weimerskirch, H., Bishop, C., Jeanniard-du-Dot, T., Prudor, A. and Sachs, G. (2016). Frigate birds track atmospheric conditions over months-long transoceanic flights. Science, 353(6294), pp.74-78.
PS: You have two questions here, specially after your edit. I suggest that you post another question regarding the spatial orientation, since asking different questions (even if they are related) in the same post is not nice, and it's a reason to close ("Too broad: Avoid asking multiple distinct questions at once"). However, it's worth mentioning that apparently birds do suffer from spatial disorientation when there is no visual cue. According to this relatively old paper, "Spatial Disorientation in Birds":

The only conclusion is that birds are susceptible and suffer from spatial disorientation, and further that the causes of spatial disorientation in birds are exactly the same as those which affect the human pilot, namely; (a) the loss of true visual cues to the horizontal; (b) inexperience in flying under such conditions where visual cues are lost;

Is anything known about how they maintain orientation? The inner ear is inadequate in the air, because it can only sense sum of gravity and acceleration and that is just the aerodynamic forces, which are always perpendicular to the wings. So how do birds know where is up without visual references?

And how does the inner ear allow detecting up? Humans certainly can't do it in aircraft. The aircraft can roll through 360° and both your inner ear and the water in the glass in front of you will both keep telling you that you are upright all the time.

I reckon that you have 2 questions here, specially after your edit. I thought my answer would be enough for you. Well, since I don't like SE posts with multiple questions (this is actually a reason to close the question: "Avoid asking multiple distinct questions at once."), let's wait and see if someone else answers this. But I believe you should ask the orientation issue as another question.


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Are chromosomal and plasmid DNA in the nucleoid?
I know plasmid DNA is not part of the chromosome, according to my textbook, but can you still class it as being part of the nucleoid?
Also is chromosomal DNA in the nucleoid?

Please consider researching your question before making it into a post on Bio Stack Exchange for elementary concepts are considered off-topic until they are supported with prior research. See help

"Nucleoid" (literally means nucleus-like), is a quite old term for "bacterial chromosome" (Better to write prokaryotic chromosome since in both type of prokaryotes i.e. Archaea (former archaebacteria) and bacteria (former eubacteria) the structure is similar).
Nucleoid structurally normally excludes the plasmid-DNA (the plasmid DNA is like additional or accessory). However sometimes a plasmid DNA could go through recombination with prokaryotic chromosome 's DNA (As seen in Hfr strain of Escherichia coli)
"Chromosome" in very brief means a structure made of DNA + Protein. In case of "bacterial-chromosome",  it contains both DNA and Protein; and if you take away the protein from bacterial chromosome; what you get, is the chromosomal DNA.

Reference:

Microbiology / Pelczar, Chan and Noel/ Edition-5;

Part 2: Bactria,

Chapter 5 (Morphology and fine structure of bacteria)

"Because it is not discrete nucleus, this nebulous structure has been designated by such terms as the nucleoid , the chromatin body, the nuclear equivalent, even the bacterial chromosome"

General Microbiology / Hans G. Schlegel / Edition-7:

Chapter-2 ; The cell and its structure:

2.2 The prokaryotic cell (protocyte) -> 2.2.1: The bacterial 'nucleus'

" Plasmids : In addition to chromosomal DNA, many bacteria contain extrachromosomal DNA in closed, circular, double stranded form. These autonomously replicating DNA elements are called plasmids. Linear plasmids have been found in some bacteria"


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How to find transcription factors?
I need to find master transcription factor(s) regulating secreted proteases in a fungus to be disrupted toward upregulation and overexpresion of extracellular recombinant proteins.
How can I detect transcription factors and preferably master TFs (master regulators) in an organism? Does NGS applicable to find TFs and preferably the novel ones? I know ChIP-seq is used to identify TF binding sites but how about detection of the TFs that bind to these sites?

How can I detect transcription factors and preferably master TFs (master regulators) in an organism?

The easiest approach to find transcription factors for any given organism would be based on sequence homology with other transcription factors. In order for this to work your organism of interest does have to be sequences, you can check this (e.g.) on the NCBI genomes page. By comparing the genome or the genes of your organism with other known (fungi) transcription factors, you can find most of the transcription factors of that organism.

Does NGS applicable to find TFs and preferably the novel ones?

Both NGS and ChIP-Seq only allow you to determine DNA (or RNA if you reverse transcribe first) sequences. Therefore these techniques alone will not help you in identifying which TFs act on your genes.

I know ChIP-seq is used to identify TF binding sites but how about detection of the TFs that bind to these sites?

I can't currently think of any 'classical' or standard experiments to determine which TFs bind to a given gene or promoter. One possibility would be to use CoIP (co-immuno precipitation) on the RNA polymerase complex and use Mass-spectronomy to identify the TFs in that complex. The problem with this is going to be, that you need a way to only get the RNA polymerase complex for your genes of interest and not all the other ones in the cell. Maybe you can use columns with DNA probes that can hybridise with your genes instead of standard antibody based CoIP.
Another way to determine which TFs bind the promoters of your genes is to analyse the respective promoter sequences. However, without knowledge of most (or at least some) of the binding sequences of the TFs in your organism, this will most likely not work very well. Edit: As @AlanBoyd commented there is a database for fungal transcription factors. However, it seems like they mainly annotate which fungi genes are transcription factors, but do not cover binding motifs of these factors.

Fungal TF database https://www.hsls.pitt.edu/obrc/index.php?page=URL1231356721

The best way is to determine the TFs in a specific organism with specific function first, then you need to check if they are transcription factors and find their domains on http://smart.embl-heidelberg.de/.

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


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What does the word "refractory" in "refractory period" refer to?
What does the word "refractory" in "refractory period" refer to?
I know what it means "refractory period" (both, absolute and relative) in the action potential graph, but I don't understand what the meaning of "refractory" in this context is. What is it refractory for?

Probably I found the answer in Britannica:

"After repolarization there is a period during which a second action potential cannot be initiated, no matter how large a stimulus current is applied to the neuron. This is called the absolute refractory period, and it is followed by a relative refractory period, during which another action potential can be generated, but only by a greater stimulus current than that originally needed. This period is followed by the return of the neuronal properties to the threshold levels originally required for the initiation of action potentials."

https://www.britannica.com/science/nervous-system/The-neuronal-membrane#ref606386

That is excellent searching. It's great that your question was answered relatively shortly after you postd it. We like and expect that all users will try to answer their own question before they post, so kudos to you.

Thank you:) Actually as usual I searched about my question and I even saw the quotation before, but just later I got the relation between the "refractory" to the things that's written there, though it is not written clearly that this is why they are called "refractory".

@UbiquitousStudent You can post your comment as an actual answer to your question and select it as the best answer by clicking on the checkmark. This closes the question and also makes it easier for the community to know the answer.

Ok, I'll do that.

From encyclopedia Britannica:

"After repolarization there is a period during which a second action
  potential cannot be initiated, no matter how large a stimulus current
  is applied to the neuron. This is called the absolute refractory
  period, and it is followed by a relative refractory period, during
  which another action potential can be generated, but only by a greater
  stimulus current than that originally needed. This period is followed
  by the return of the neuronal properties to the threshold levels
  originally required for the initiation of action potentials."

Absolute refractory period = initiation impossible absolutely
Relative refractory period = initiation possible but in greater energy relative to the original required.


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Accumulation of Na⁺ and Ca²⁺ in the myocardiocytes while having acute heart failure
Why is it necessary to have accumulation of sodium and calcium ions in the myocardium cells while having acute heart failure? Normally, at resting membrane potential, sodium and calcium are more outside of the cell than inside, then I expect to see them enter less to the cell than to expect from them to enter and not exit.

Maintenance of resting membrane potential is an active process and you need energy and intact cellular membrane, otherwise the ions will flow in the direction of their electrochemical gradient, in this case into the cell.

Thank you^ Basically, If I understood you properly, you've said that in this case the cellular membrane is non-intact or damaged. How the non-intact cellular membrane is expressed in this case?

I meant to ask also How the non-intact cellular membrane is expressed in this case? and why it happens in heart failure? I thought about MI, but maybe it's not necessary.

@UbiquitousStudent the condition is energy and intact membrane, Since the word and is used it is understandable that violation of any one term, there will be failure.


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How did Portuguese man-of-war evolve?
In particular, how did the close cooperation of its many component species evolve?
My hypothesis is that it began with a few, probably no more than two zooids cooperating in symbiosis, and overtime, either entirely new species of zooid adapted to first parasitize and then cooperate with the existing company, or that some of the existing zooids mutated to acquire different functions. As the new zooids join the cooperation, the other re-adapt to form the "species" we see today.
Is that a somewhat accurate description of the evolutionary history of this colonial organism?
Addendum:
Would the relative simplicity of the polyps forming the colony be a crucial prerequisite in their cooperation and specialization?

Isn't it the case that various types of zooid are actually all the same species?

Googling 'Origin of Polymorphism in Cnidaria/ Siphonophora' should help you.

@AlanBoyd If so, are polymorphic individuals differentiated by epigenetic mechanisms? Also, would the difference between individuals of various functions be "discretely" differentiated (like the difference between queen ant and worker ant) or "continuously" differentiated (like the difference between leaf-cutter ants of various sizes)?


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How does entry of Ca²⁺ to the myocardiocyte make it more contractible?
I'm trying to understand why an increase of Ca2+ entering into the cell, increases the force of the heart contractions. Based on what I have watched in many lectures videos on Youtube (this one- "interactive biology" for example on 4:45), Ca2+ basically slows the repolarization in phase II of the action-potential membrane, and I don't understand how it does the cardiac cells more contractible. Or maybe the answer is pinned in the words "typical cardiomyocytes" and then I didn't get it.

The answer is a bit more complex. Calcium ions have a lot of effects in the cardiac myocyte. Apart from the increased contractility (positive inotropy), extracellular calcium concentration also alters chronicity as you mention by altering the rate of repolarisation. An attempt at a simplified picture of the inotropic effects follows:

First is to increase the contractility via directly sensitizing the tropomyosin system. Have a look here. Quoting the paper, "...In both cardiac and skeletal muscle, the force-generating molecular motors (crossbridges) are turned on by increasing the intracellular free calcium level that regulates the troponin-tropomyosin system. However, calcium activation is a two-way process in the sense that activated crossbridges also affect the troponin-tropomyosin system...An increase in Ca2+ activity causes an azimuthal shift of tropomyosin around the filament (by about 30 degrees), thereby increasing the probability of low-force crossbridge interaction, a process which by cooperative effects induces further tropomyosin movement (by an additional 10 degrees) which results in the open state of the filament characterized by forceful cross-bridge interaction...". Hence, higher the intracellular concentration of Calcium, greater is the maximum force.
Sarcomere length also affects the sensitivity to calcium. This increase in contractility is not because of calcium but is mediated by calcium. The reason has something to do with lateral filament lattice spacing decreasing, increasing the probability of cross-bridge formation, increased strain on titin alters lattice spacing and myosin packing.

As I said, this is a bit too oversimplified. There a lot of inter-regulations taking place. Have a look at these papers here.

Myofilament Calcium Sensitivity: Role in Regulation of In vivo Cardiac Contraction and Relaxation (A good review plus a bit of quantification on the topic being discussed)
The negative inotropic effect of calcium overload in cardiac Purkinje fibers (To present the complexity)

Two different but related processes i.e excitation- contraction coupling could possibly answer your question. Please see the simple diagram:
https://image.slidesharecdn.com/heartcirculation-120511091224-phpapp01/95/heart-circulation-47-728.jpg?cb=1336727680
 "Ca2+ basically slows the repolarization in phase II of the action-potential membrane" what you said is one of the excitation phase during which Ca2+ influx cause more Ca2+ release from endoplasmic reticulum, increasing Ca2+ concentration in the cytoplasm leading to more binding of Ca2+ to troponin C and subsequently increase force of contraction.


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How exactly are genes swapped during the process of recombination?
I am studying recombination in Meiosis and the idea of crossing over doesn't make sense. My understanding is that 46 chromosomes in our germ-cell (23 from mom + 23 from dad) line up next to each other and recombine (swap areas of DNA). My confusion is that, since, for example, Chromosome 1 from mom is same as Chromosome 1 from dad, how is swapping areas of DNA going to exchange any information. Brown eye gene from dad would just be swapped with brown eye gene from mom. How will have any affect on the offspring? OR is it that if mom has brown eyes, the brown eye color gene in mom has something attached to it?
OR is my understanding of genes incorrect and not every nucleus has all possible genes? (except the difference of X and Y chromosome.)?

The chromosomes are not equal. Read about alleles first before you start reading about recombination.

And please change your title since it bears no relation to your actual question.

@adjan thank you for your suggestion! So, one person has a form of a gene and not ALL forms of all genes. This clarifies a lot.

There is quite a few misunderstanding in your question. So, I'll shortly give you some (simplified) definitions and then point you to another post.
Definitions and Basic Concepts
A locus (plur. loci) is a position along a chromosome. A some loci, there are  genes. To make things easy a gene is any sequence which is transcribed into RNA and translated into proteins.
Now at any locus, you might see different individuals having different variants. For example an individual may have the sequence ATTCT while another individual may have the sequence ATTGT. Those different variants are called alleles. It is key to understand that there is genetic variation in populations. This genetic variation is a big part of the reason why people around you look different and why you ressemble more your siblings (if you have any) than a random person in the population.
How does recombination have any impact?
To understand the effect of recombination you necessarily have to picture a several loci model. As you now understand the above definitions you will find your answer at this post: Why do we need two markers to measure a recombination rate?
Further readings
The following posts will also be of interest to you:

Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?
Chromosome and chromatid numbers during cell cycle phases

Thank you. My main misunderstanding was that same chromosomes in all individuals is exactly the same. I now understand that there can be different forms of a gene (allele). Not all people have all forms of a gene.

Cool. There is indeed genetic variation in the population. This is a big reason for why we look different. Note that have understanding the existence of genetic variation and its maintenance in populations is key to have a basic understanding of evolutionary processes. If you think I answered your question you can check the checkmark to the left of my answer.

My question now is, "Do all genes get transcribed then?" I remember reading that only a percentage of DNA is transcribed. When I read that, I thought maybe if you have blue eyes, only blue eye gene would be transcribed and genes for all other eye color would be "trash DNA". But since you only have one gene for eye color, and same with all characteristics, what part of DNA does not transcribe? I hope my question is not too confusing.

We typically define a gene as a sequence that gets transcribed. So, by definition, yes all genes get transcribed. But most of DNA is not made of genes. There are regulatory sequences and introns (~24%), there are pseudogenes, there's loads of transposons and retrostransposons (~60%) such as the ALU sequences. "Junk DNA" is some kind of an undefined term that encompass all the non-coding DNA (~ 98.5%) but the term "Junk" has been very misleading to the large public. Of course all of this is not so specific to humans. Plants typically often have very large genome with loads of transposons.

Anyway, your follow-up question is very broad. You should just follow an intro genetic class or read some wikipedia articles and try to come back with a more narrow and accurate question. Good luck exploring this fascinating field of knowledge!

That was actually a perfect answer to my question! Thank you so much.

Let us continue this discussion in chat.


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Why would eating the meat of cows fed with antibiotics trigger an immune response to the antibiotics?
The document "Antibiotics and Antibiotic resistance" contains the following paragraph:

The indiscriminate use of antibiotics in feed stuffs means that humans
  may receive unwanted doses of antibiotics in meats, eggs and milk.
  This exposure may cause the development of an immune or inflammatory
  response to the antibiotic so that the human cannot be treated with
  the drug at a later date. The practice has also resulted in the
  development of antibiotic-resistant strains of bacteria.

Here are my two questions that test general biology principles:

How can there be an immune response to an antibiotic?
I think that the answer to the first question will answer this one anyways, but for the sake of completeness: why would the immune response to an antibiotic prevent the antibiotic from being used again? (I may know how to answer this once I actually know what an immune response to an antibiotic looks like.)

How can there be an immune response to an antibiotic? Because it is a foreign molecule. So people can develop an allergy to it (there are quite a lot of people allergic to penicillin and it's derivates).

So do antibiotics count as antigens in that sense? I believe that antigens are any substances which have the capability of triggering an immune response...

The antibiotic or some product of metabolizing it might be an antigen.

It's difficult to know how to answer this question because it is unclear why you think that this might not happen.
As skymningen has said in comments, any foreign molecule is capable of acting as an antigen,  in principle. We know that people develop allergic reactions to penicillin. And if you do a Google search for immunoassay [insert name of antibiotic] you will probably find results indicating that there are commercially-available kits for assaying the antibiotic based upon antibodies directed against it.
It is however worth noting that these anti-antibiotic antibodies were certainly not raised directly by feeding, or even injecting, the antibiotic. This is because the immune system doesn't really respond to small molecules. If you want to make antibodies directed against a small molecule you have to tag it on to a protein - this is called haptenisation. Then some of the antibodies that develop against the modified protein will recognise the hapten (the small molecule). Another example of this is the development of immunoassay for steroid hormones.
So we have to imagine that a fed antibiotic enters the bloodstream and then reacts chemically with a blood protein - essentially the antibiotic has haptenised itself. I seem to recall reading that β-lactam antibiotics are fairly reactive against lysine residues. The propensity of different antibiotics to provoke an immune response may be simply a function of their reactivity.


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Can someone identify this ant queen?
I know it's kind of hard to see but can anyone tell what it is?

Sorry, but this is so blurry had a hard time to find the ant at first sight. Please try to get a better picture and add information about where you found this ant, otherwise it will be unlikely someone is able to identify it.

I found this ant in my backyard in North Carolina when I get home I'll get a better pic.

How do I add another pic?

You can edit your post.

[edit] to edit.


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Chemical methods to detect cell division
So I have been working on a project for a while, and there is one mechanism that I need a little bit of advice about.
The project is chemical-biology based, so don't be deterred :)
Theoretically, by this point in the experiment:
I put cells (let's say lymphatic or endometrial) into stasis, through means of lyopreservation, and now, I have brought them out of stasis, through exposure to a sucrose (trehalose)-based medium.
Now I am attempting to chemically detect mitotic growth within the cells, how can I do this?
This is where the chemistry comes in: My first thought was to use a chromatic indicator that would fluoresce or irradiate in response to mitotic acceleration, but I have not yet found a suitable chemical. In research, I found that a similar experiment had been done in bacteria, and the chemical dimyristoylphosphatidylcholine (1,2-Dimyristoyl-sn-glycero-3-phosphocholine) had been used. Would this work in mammalian cells? Another idea was to use a chemical that detects the unnatural growth from the spindle fiber and centriole point of view, reacting when the centrioles entered the phase to replicate. I have been unable to find any chemicals that make use of the replication of centrioles, or the spindle fibers, so I need ideas.
To summarize: Does anybody know of any biochromatic indicators that react through detection of rapid, mammalian, mitotic growth? Not necessarily cancerous and uninhibited, but rapid meaning 'a speed of mitosis that is faster than the norm.' Preferrably, the indicator would be able to stay in stasis for extended periods of time.
If such an indicator is not available (or you do not believe so) then does there exist a biochromatic indicator that reacts in the presence of any sort of cell division?
Is there a way to chemically detect cell division?
I am welcome to all ideas.

There is one important experimental detail missing: do you want to 'keep' the cells you measure growth in, or can they die as a result of the measurement?

They can die, but only after it has been determined whether or not they were growing.

There are many methods to study the cell cycle, and it's not clear to me exactly what you want to measure. What do you mean by "mitotic growth"? Mitosis is a specific event in the cell cycle (separation of chromosomes), are you attempting to detect mitosis events specifically? This is distinct from measuring DNA synthesis, or merely the DNA profile as @Nicolai suggests, which would rather indicate proportions of the cells in the difference cell cycle phases. Cell growth is also different from proliferation. Please clarify.

I desire a chemical which would change color in the presence of cell division, at the bare minimum. Specifically, it would be nice to detect if cell division was faster than normal. Whether this is done through DNA or telomeres, I have no preference.

The most common indicator for the growth of any kind of cell (population) I know of is the amount of DNA in that cell. There are a number of (fluorescent) dyes that bind to DNA in a stoichiometric fashion and can therefore be used to determine the (relative) amount of DNA inside a cell (is hope that's what you mean with 'biochromatic indicator'). The most common dye used in this way is probably DAPI.
In order to determine which cells are dividing, you'll obviously need a device that can measure the fluorescence of each cell individually- so either a microscope or a flow cytometer. Because growing mammalian cells (it seems to me that's what you want to look at) multiply their full set of diploid chromosomes in the S-phase of the cell cycle, you can discriminate growing cells from others by their relative DNA amounts:

A non-growing cell has only the diploid chromosomes (1x relative DNA)
A growing cell will have either the doubled set of chromosomes (2x relative DNA) if it sompleteded S-phase or an intermediate amount (1-2x relative DNA) if it's currently in S-phase

Figure 1 of this (really old) paper also shows, how DNA amounts can indicate at which point of the cell cycle a cell is (which tells you if its growing) works.
A note on cell viability:
Staining any kind of cell with DAPI (or most other dyes that bind to DNA) will most likely kill it or at least act as a very strong mutagen. Based on your answer to my comment this should not be a problem.
While not really part of your question, you mentioned that you want to preserve cells using lyopreservation, which basically means drying them. You should consider, that mammalian cells will most likely not to survive this process (unlike plants and some invertebrates there are no mechanisms in mammalian cells to protect them against the water loss). Without sorting the live cells from the dead ones first, your measurements may detect cells that were dividing prior to the preservation.


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Is the water-splitting enzyme a component of photosystem II?
Can Somone answer a bit bizarre question which is that in light reaction . Photosystem uses enzyme to split the water up to hydrogen ions and electrons and oxygen.But is this water-splitting enzyme in or out of the photosystem 2(PS II)?
Great thanks

where have you looked for answers to this question? Can you give a bit more background?

The name of the protein (actually, three proteins) you are referring to is Oxygen-evolving Complex.
And yes, it is part of Photosystem II.
According to Lodish (2002):

An Oxygen-Evolving Complex in PSII Regenerates P680: The splitting of H2O, which provides the electrons for reduction of P680+, is catalyzed by a three-protein complex, the oxygen-evolving complex, located on the luminal surface of the thylakoid membrane. The oxygen-evolving complex contains four manganese (Mn) ions as well as bound Cl- and Ca2+ ions (see Figure 16-44); this is one of the very few cases in which Mn plays a role in a biological system.

You can see the complex in this diagram of PSII, also from Lodish:

Figure 16-44: In a reaction center, two integral proteins, D1 and D2, bind the special-pair chlorophylls (P680), two other chlorophylls (Chl), two pheophytins (Pheo), one Fe atom, and two quinones (QA and QB). All of these are used for electron transport following light absorption by an associated lightharvesting complex (see Figure 16-42). Three extrinsic proteins (33, 23, and 17 kDa) comprise the oxygen-evolving complex; they bind the four Mn2+ ions and the Ca2+ and Cl− ions that function in the splitting of H2O, and they maintain the environment essential for high rates of O2 evolution.
As you can see, all proteins coloured green in the image above are part of PSII. However, since the oxygen-evolving complex is made of extrinsic proteins, it can be easily separated from the rest of PSII:

The Mn ions together with the three extrinsic proteins can be removed from the reaction center by treatment with solutions of concentrated salts; this abolishes O2 formation but does not affect light absorption or the initial stages of electron transport.

Source:

Lodish, H. (2002). Molecular cell biology. 4th ed. New York, N.Y.: Freeman.

Greatly Thanks!By the way can u cite this information for me?

What do you mean by "cite this information"? The reference is at the end of the answer.

Oops sorry I forgot to see that

I too have just been studying Photosynthesis :)
From what I understand the PSII is the enzyme that splits water. Water splitting occurs in PSII. In that case what you could further ask is where in this big enzyme does it take place?
Basically the PSII is composed of many protein-complexes and pigments. One of them known as the oxygen-evolving complex (you can read more here: https://www.google.co.in/?gfe_rd=cr&ei=3AgsWd2VMunn8AezuYqYAQ#q=oxygen+evolving+complex) is the site in PSII where the water splitting takes place.
You can also study about photosynthesis here (https://www.khanacademy.org/science/biology/photosynthesis-in-plants).
Hope it helped!


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PCR related problem
Recently, I have done a PCR of a region of human p53 gene and got faint band after that. Then I used that PCR product as input and did a nested PCR with same PCR condition, but now the specific band disappeared and only smear was there. Can anybody help me to solve the problem. Why that happened and what should I do to get specific band.

Can you tell us what the template DNA was in the first PCR?

More detail of both protocols would be helpful.

Ther could be different problems affecting your r salts. Maybe the primers you are using are not specific enough or your PCR condition are not optimal. I would first check the primers by blasting them against the human genome to spot mismatches. If your primers do not bind uniquely to your gene of interest then design a new pair. If the primers are ok, then I suggest you to run a grandient PCR (annealing temperature from 50 to 65 degree Celsius) to determine the optimal annealing temperature of your primers. These two steps usually solve 99% of my PCR problems, assuming that your template DNA is ok and at the right concentration. If even with the gradient PCR you can't find a good condition, the next step is to play with the buffer by changing magnesium chloride concentration and maybe adding betaine.


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Why did black swans to evolve black colouring?
What environmental factor caused black swans, which are native in Western Australia, to evolve black feathers ? Note swans are either black or white, there are no brown or grey colurings, which can be commonly found in various geese and duck spieces.

Because somewhere, sometime in the distant Australian past, either it helped them hide from, or deter, predators and/or helped them hide from prey increasing their chances of feeding and/or made them attractive to others and/or somehow a gene linked to color conferred some quality which increased their chance of survival. You missed the Black Necked Swan.

Also, is there any disadvantage in having black feather? Because characteristics like "the color of something" may just appear by simple point mutation and stay if not counterselected. Often they have a social effect, for example it's easier to recognize your pups if they have a different color.


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How can just new born baby can walk ?
This website here stating video of New born baby walking breaking the internet.
How can just new born baby can walk ?

Just a stepping reflex: https://en.wikipedia.org/wiki/Primitive_reflexes#Walking.2Fstepping_reflex . That's it, too much internet for today, i'm gonna read a book... (PS: I speak portuguese, and that midwife seems very surprised. I believe she is faking or exagerating, because she should know that this is a normal reflex).

The baby isn't walking exactly. It can't support it's own weight. It's stepping: moving its feet in a step-like fashion when the tops of the feet are brushed against a surface or placed on the surface, a primitive reflex like the Moro Reflex, present in all normal newborns.

@anongoodnurse are you saying website is wrong?

@GerardoFurtado - I've tested every newborn I've delivered or taken care of, and I have to admit this one is impressive, if only because 1) the baby is being held aloft so long and effortlessly by the...person, and 2) the baby usually gives up after a few 'steps', at least, I gave up then, as the point is not to see how long they can do it, but that it's there. So, all in all, it's a fun vid. Don't rag on the midwife. I would have commented as well, and I've seen it hundreds of times.

@DhanrajKumar - I didn't say anything about the video or the website. You see what you see. I'm explaining what is happening.

@anongoodnurse Yes, it's impressive, but they (both of them, the midwife and the person who's filming, which I believe also work at the hospital) are talking like this was never seen before.

@GerardoFurtado - Well, then, I agree with you. It's for the camera, I guess.

@anongoodnurse Actually, to be fair, I just watched it again, the person surprised is the person filming, and maybe she is not aware of this reflex (or she's aware, but was excited). The only thing the midwife/nurse says is "she walked from here to there... I was about to give her a bath". So, the midwife is not that impressed.

@GerardoFurtado - That makes sense. I don't understand Portuguese (wish I did), but it sounded to me like an excited grandma ("Oh, look at what my beautiful, talented, miraculous new grandchild can do!" kind of thing. Nice of the midwife to give grandma such a sweet treat for posterity. (Grinch that I was, I would have been more concerned with getting the baby dried off/warmed up.)

Yes, it's probably someone from the family, a grandma or an aunt! By the way, I'm seeing several websites translating the conversation, with expressions like "heavens above", "good lord" etc... they (the nurse and the grandma) are not saying that this is a miracle, those are common expressions in portuguese (spoken even by atheists)! Good on you, being worried about getting the baby dried off/warmed up... but since this is a preparation for a bath, it's probably several hours after the birth, or even a day later, isn't it?

@GerardoFurtado - Don't honestly know. Still has a lot of vernix (caseosa) on it. Lots of it wiped off. Could be a few hours, yes.

@DhanrajKumar- http://www.techtimes.com/articles/208562/20170529/watch-video-of-newborn-baby-who-tried-to-walk-immediately-after-birth.htm


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Flow cytometry data Analysis
everyone.
Since I am new in the flow cytometry technique, I am not really sure how to analyze the result.
We use cell U-937 Lymphoblast.All Cells

Could Anyone help to explain me this one?
Thanks in advance!

Please explain what your study is about. We can't just guess what you are doing

Disclaimer: Assumes you know how flow cytometry works.
You've done a flow-based AnnexinV apoptosis assay here.
Annexin A5 (AnnexinV) protein binds to phosphatidylserine (PS), which is typically in abundance of the inner leaflet of live cells. Upon the initiation of apoptosis, PS is known to flip to the outer leaflet. Thus, you can use AnnexinV conjugated to a fluorescent molecule such as fluorescein isothiocyanate (FITC) to look at externalized PS.
7-Aminoactinomycin D or 7-AAD is a fluorescent intercalator that can be used to detect DNA and is excited on the 488nm laser (emits on a 650nm longpass filter or the like). The dye is not permeable to live cells, and so for dead or dying cells with compromised membrane permeability, it binds freely to DNA.
The problem with either alone is you cannot say a 7-AAD+ cell is apoptotic and you cannot say an AnnexinV+ cell is apoptotic, because we know that you have early apoptosis and late apoptosis, and in either the cell isn't wholeheartedly dead, yet. You also have necrosis.
And so on a dot plot of 7-AAD and Annexin V, you can create 4 quadrants based on the mechanism of the two components:
Double-negative: No external PS or DNA binding means these are viable cells.
Double-positive: Both external PS and membrane instability means late apoptosis.
AnnexinV single-positive: Undergoing early apoptosis, nucleus isn't yet permeable.
7-AAD single-positive: Completely dead or necrotic, membranes have probably disintegrated.

The basis of the assay is you're trying to determine at what stage of cell death your cells are in.
The unstained control is a way of looking at your cells alone, and allows your to correct for autoflorescence, florescence generated by your cells just from excitation alone. You also want to run single-stain controls to see where your positive, and negative populations lie. Without FMO (fluoresence minus-one, basically your full staining panel minus a color) controls, it's hard during gating to confidently say where your positives and negatives are delineated, due to the effects of spillover and noise.
A note about the AnnexinV single-stain control: You can see that in the untreated sample, there's basically no AnnexinV, but in the control it's 22.0% of the cells. Single-stain controls where you assume positives exist have to have positive and negatives. Without positives, where do you set the gate for them? What if the population shifts during acquisition? They probably used cells that were dying on purpose to generate confident controls for that sample.
That's the left half of your data. The right half are treatments. Basically you've stained the cells for both markers and then treated them with Torin2, Rapamycin and Mitomycin to see how those compounds affect the viability of the cells. There's a control where you added nothing.
Based on the gates set with the controls, you can see that the mitomycin sample has the greatest effect: The cells are 6.54% AnnexinV positive, undergoing early apoptosis, and 14.3% are double-positive, undergoing late apoptosis, and 8.09% are dead or necrotic.
The conclusion you'd derive is that mitomycin, but not the other compounds, has a profound effect on the viability of the cells.

Thanks So much for your explanation. I did learn a lot from you. :-) @CMosychuk

And in the 7-AAD single staining, we did not put Annexin V, why we can see the amount of cell death in the annexin V quadrant?

The laser is still collecting in the annexin channel, the author simply didn't stain that marker. So it could just be noise, or autofluorescence, or spillover in some cases (I don't know what fluorophore they used to stain annexin). If you saw something significant there, you could subtract that background from your treatments to get a more accurate readout.


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Immune system initial response
One thing i can not still comprehend about the immune system is the following:
A bacteria is first recognized by neutrophiles. But then neutrophiles have to have the ability to release chemotaxines upon the recognition (or the bacteria?)? Its not mentioned anywhere in my script how macrophages and other non abundant innate immune cells come to the source of an infection in details.

Have you looked into the role of the complement system? It generates cytokines. In fact those molecules play a role in attracting neutrophils.

On the contrary it's not neutrophils that initially recognize a threat, but rather distressed epithelium, and immune cells like DCs or macrophages that are already distributed in the tissue that recognize pathogen- or damage-associated molecular patterns (see PAMPs and DAMPs). The primary response to these patterns is the secretion of cytokines.
Among the many cytokines secreted include a subset known as chemokines, from the Greek work for movement. The combination of chemokines and cytokines induce chemotaxis of immune cells circulating in the blood, such as neutrophils, by telling these cells that the nearby tissue is inflamed. IL-1ß, IL-6 and CXCL2 are examples of neutrophil attractants secreted by macrophages and monocytes. Complement fragments like C5a are also known to induce an inflammatory response, inducing the secretion of these molecules.