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How interrelated are computational biology and biophysics?
I am considering applying to Ph.D. programs, and am not sure what direction to take. I'm hoping you all can help me out.
I have a background in both biology (molecular focus) and physics (condensed matter and math, heavy on theory). Several years industry experience working in labs doing molecular biology and genetics research.
My primary interest is in mathematical modeling of biological systems, and taking this knowledge to then engineer function. Essentially, what I view as a combination of biophysics, systems biology, and synthetic biology.
Here is the dilemma. It is important for me, should I pursue a Ph.D., to have a solid foundation and training in fundamental principles in physics and math, because I want to be able to derive new theories, models, and methods when needed. This leads me to think biophysics or applied math is the "right" area to do my Ph.D in. But biophysics is very broad and systems biology is only a small part. It is also removed from applications in bioengineering.
I know computational and systems biology intermingles biophysics, applied math, genetics, computer science, and various other fields. It also seems like the type of research I am interested in is typically done in computational and systems biology groups. But I'd like to know if computational biologists, aside from doing simulations, also commonly do work in deriving new models/theories in biophysics. Or do they generally apply this knowledge to build simulations and understand data sets (i.e. removed from fundamental biophysics research)? I don't want to be a programmer -- I want to be a theorist who uses computational tools (and only programs when it's needed to simulate something) to solve problems that can't be solved analytically.
Is computational and systems biology an appropriate "umbrella term" for what I'd like to do? Or would I be better suited in a physics Ph.D. program, and attempt to bridge that training towards systems biology research?
Also, how difficult is it to change to a related field if the opportunity arises? Can computational biologists, who are also interested in engineering work, build a model of a system and then work with others to help engineer it?
My overall concern is pigeonholing myself into a field that I don't want to spend decades working in. I want to maintain flexibility along the range of biophysics to bioengineering, and work on problems when the need arises. Also, what field do my research interests actually fall under? I find it often depends on the university and specific department, so it's a hard question for me to answer myself....
Thanks in advance for any input.

Computational Biology is just the application of computers to solve problems in biology. It may mean using machine learning to identify regulatory regions in DNA or it may be solving a complex system of differential equations to model chemical reactions in some metabolic pathway. Whether a background in physics, chemistry, biology, math, or computer science is more central depends on the exact problem you want to work on,  and in fact which aspect of the problem you want to work on.

Also, what field do my research interests actually fall under? I find
  it often depends on the university and specific department,

Bingo! Your interests are clearly cross-disciplinary, so for any given research question, different researchers in different fields will all be working on different aspects of the problem. Academic disciplines don't get to declare monopolies on research problems!
You Ph.D. is going to require you to spend 4-6 years working on a VERY specific problem. It would be wonderful if you could figure out exactly which research problem you wanted to dedicate the next 6 years to, and then choose the Ph.D. program based on their research program on that problem. This is rare though. More typically Ph.D. students have to spend a year or two doing rotations and talking to potential mentors before picking a research problem. In that case you are going to have to decide which academic discipline attracts you more, and then find a department in that discipline that seems to have a lot of collaborations with the other disciplines that attract you. See Buridan's Ass;

Thank you! Just the response I was looking for. I actually do know the problem I want to work on. I want to take a biological system (currently working in the agriculture industry; so take plants in this case, but I am open to others) and apply systems biology methods to better predict phenotype, and figure out what parts need to be changed/engineered/modified to drive the plant (or other system) to a desired state (e.g. disease resistance). But, a "big picture" answer to this may require new applied math (graph theory) or biophysical (statistical mechanics) methods that aren't known yet.

But I "don't yet know what I don't yet know", if that makes sense. So is it better to go more fundamental? (biophysics --> statistical mechanics, applied math --> graph theory, group theory) Or more applied (computational biology, systems biology)? Intellectually I think I'd rather go more fundamental and transition to applied/computational (I think it's harder to do the converse). But I really think this may be limiting future job opportunities (who would hire a biophysics phd for a computational job when you have a computational biologist phd to choose from)?

(i.e. it's not just a "what am I interested in" question, but also "how do I get a stable job at the end of my Ph.D. question) Which makes it way more complicated. :(

'So is it better to go more fundamental? (biophysics --> statistical mechanics, applied math --> graph theory, group theory)' There is no general answer to this. It depends entirely on the problem and your personal tastes.

"it's not just a "what am I interested in question, but also but also 'how do I get a stable job at the end of my Ph.D. question) Which makes it way more complicated. ' That's a separate question from the one you asked. Keep in mind that Stackexchange is a Q&A forum, not an open-ended discussion forum. Use the chat facility for open-ended discussions. Right now demand is high for machine learning and 'data science' experts across a variety of industries. Whether that will be true in 6 years, no one knows. No one can give you guarantees on this, other than that jobs in academia will be tight.

"That's a separate question from the one you asked. Keep in mind that Stackexchange is a Q&A forum, not an open-ended discussion forum. Use the chat facility for open-ended discussions." Yes -- sorry about that. Wasn't aware of the chat facility. The "can I get a job doing this" was an important corollary to my question. I want whatever I choose as a dissertation and subfield to be employable in the range of research fields I'm interested in, if that makes sense.

I feel like systems biology, and by extension (since they're often grouped together in a department) computational biology, makes the most sense. As I don't necessarily even know what new models or mathematics needs to be used or created until I get to that point in systems biology. Putting the cart before the horse and all that. Anyway, thanks for the help and sorry for the segue into the open-ended discussion.


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Biological EM emissions
What sorts of EM frequencies are emitted by the human body?
Are there any processes in the human body that produce Radio/Microwaves or uv/x-rays/gamma rays?

have you googled this at all?

I agree with @aaaaaa's comment but the downvote is a bit much in light of the user's newness to the site, IMO.

i will upvote when @bobiscool add  results of some research and mention may name in comment (so i can see).

https://io9.gizmodo.com/how-much-radiation-does-the-human-body-emit-1719085023
This confirms part of my question, radioactive isotopes can be mistaken for needed materials in the body.

@bobiscool: aaaaaa would not get your comment unless you use his username. I added your link to my answer and found a paper and discussion that also support the premise of your question.

According to this author (1) the human body emits radiation, mostly in the infared region. Human body temperature generally exceeds that of its surroundings and so there is a net flow of heat from the body into the environment, some due to convection and some due to thermal radiation.
This Czech paper suggests (2) human EM emission in a particular low-frequency band (0.5 - 30 Hz), but the writing is awkward and I do not think this is peer-reviewed.
A more comprehensive Russian paper (3) discusses, among other things, emission of photons (light!) from human skin. The energy of this light is not very high (1-3eV, which is 1-3 times $1.602~ \text{x}~ 10^{-19}$ Joules), but it's not nil.
This interesting topic has been studied extensively and this is a quick glance. Am adding the link furnished in a comment by OP above which does suggest that the body can emit energy via radioactive decay.
Also, this link (4) based on the paper by Toohey below discusses radioactive emission by humans in some detail, including radioactive decay of potassium-40. There is apparently a mechanism by which ambient gamma radiation can interact with atoms in cells (photoelectric effect) to produce x-rays, which are emitted from the body.
(1) Olivia Lee, Hong Kong Observatory, Sept. 2010
(2) Lipkove, Cechak, Human Electromagnetic Emission in the ELF Band,Measurement Science Rev. vol. 5 sec. 2, 2005
(3) Ignativ et al., Fields in the Electromagnetic Spectrum Emitted From the Human Body..., J. Health, Medicine and Nursing, vol. 7, 2014
(4) Toohey RE, Keane AT, Rundo J. Measurement techniques for radium and the actinides in man at the Center for Human Radiobiology. Health Phys. 44(1):323–341; 1983.

Do the neural processes which produce electrical "noise", such as that detected by ECGs and EEGs, produce any EM radiation at all, or are they not coherent enough for that?

@Watercleave: The short answer is, only locally (doesn't radiate). See, for example, https://www.quora.com/At-what-distance-can-brain-waves-be-detected.

1-3eV light sounds like infra-red radiation (heat dissipation basically). Not sure about photons of visible part of the spectrum though. However, there is intrinsic fluorescence so that photons get emitted when tissue is being hit by photon of shorter wavelength

@aaaaaa: visible spectrum emission was news to me and was surprised that reliable measurements could even be made of energies this small (on a human--vs. some purely mechanical system).

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Need to identify this insect and ways to eradicate it
I need some help in identifying this unknown insect that was found in my kitchen.
Thanks in advance.

It might help if you added localization and size information.

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What is this insect? Seems to be in Indonesia
https://www.facebook.com/gadik63/videos/707361412787259/
This video has me completely baffled.

https://en.wikipedia.org/wiki/Creatonotos_gangis
Creatonotos gangis is a species of arctiine moth found in South East Asia and Australia. It was described by Carl Linnaeus in his 1763 Centuria Insectorum.


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Why are there so few multicellular anaerobes?
There are a few documented cases of multicellular anaerobic organisms, but I can't see a reason for it to not be more common. On the contrary, it seems pretty useful to be able to create energy even when deep inside tissues, yet the Loricifera are the only ones I've found documented. Given how often multicellularity has arisen, is there something that's fundamentally difficult about being anaerobic while multicellular?
One thought that might inspire others- multicellular organisms certainly tend to be bigger than unicellular ones, and in an oxygenated world larger organisms are more likely to run into oxygen than unicellular ones. However, there still exist an abundance of anaerobic niches for large organisms- the deep sea, for example.
I'm also drawing a distinction between facultative anaerobes and obligate anaerobes- there are plenty of facultative multicellular anaerobes, and I'm not as curious about that.
Useful sites that I came across while searching:
Journal article announcing the first anaerobic metazoa
Anaerobic fungi, presumed to be unicellular?

keep in mind even the deep sea can still have significant oxygen levels.

Fascinating question. I don't know the answer, but one possibility is that multicellularity required other inventions of the eukaryotes (more complex gene regulation, for example), and the fact that eukaryotes have mitochondria is just a co-occurence, not the driving factor.  Btw, the Loricifera species apparently has hydrogenosomes, which are thought to have evolved from mitochondria, but have lost respiration. Many parasitic species have similar non-respiring mitochondria-like organelles; see for example http://rstb.royalsocietypublishing.org/content/365/1541/713.long

I would think it would be a result of energy demands. Aerobic respiration yields more energy per molecule of glucose than aerobic respiration. So for a multiceullular organism, it will be easier to satisfy the high energy demand that multicellularity can create, especially in organisms like mammals that maintain a constant body temperature and have a complex and metabolically expensive brain. I know some plant tissues and tumors will sometimes use anaerobic respiration when they are in low oxygen environments, but the energetic benefits of aerobic respiration may be too good to pass up.

Simple answer: very little oxygen is required for a decent amount of energy, and very little carbon dioxide is given off. These are also both gases, which makes distribution a good bit easier. Take ethanol or lactic acid fermentation. Every cell producing that byproduct at once would result in an insane amount of waste to concentrate and excrete, and a huge amount of it would be required. Because of this, anaerobic species haven't had much evolutionary pressure to become multicellular, even if it would be technically possible.

I did a bit of reading myself, and it seems as if Loricifera are the only multicellular obligate anaerobes.
I see your point with niches for anaerobic organisms in deep water. Many organisms near the hydro-thermal vents use anaerobic cellular respiration.
From my understanding of Loricifera, it seems as if they would utilize chemosynthesis as their method of obtaining energy.

Loriciferans are found exclusively in marine habitats, and live in the spaces between sand grains or in the mud at the bottom of the deep sea. The nanaloricids prefer sand with low levels of detritus (material derived from the decomposition of once-living organisms) or clean shell gravel, whereas the pliciloricids are often found in such deep-sea sediments as the white abyssal Globigerina ooze and the red deep-sea clay from the hadal zone (below 20,000 ft; 6,100 m).

--From Encyclopedia website: Loricifera (Girdle Wearers).
Lociferans live in a rather oxygen-less environment.

So you're right about niches in the deep sea.
But typically the deep sea has extremely high levels of pressure that few multicellular organisms are built to handle.
Additionally, I was able to find a few other obligate anaerobic Eukaryotes, but those were Protozoa, so thereby not unicellular.
About it fundamentally being difficult to be exclusively anaerobic while multicellular, with multiple cells, there is more upkeep and more energy is required to run the "system". Aerobic processes tend to be a lot more efficient, producing more ATP for usage.

Only 1 ATP (from my understanding) is produced from this, whereas with aerobic respiration:
Aerobic ATP sum
Much more ATP is produced from aerobic processes.
In the end, the majority of obligatorily aerobic organisms are unicellular, or are extremely small.

Their sizes range from 100 µm to ca. 1 mm.

So... that's why multicellular organisms are typically carry out aerobic cellular respiration.
Also, about the fungi you mentioned, it goes through Horizontal gene transfer, which unicellular organisms typically use:

Horizontal gene transfer (HGT) or lateral gene transfer (LGT) is the movement of genetic material between unicellular and/or multicellular organisms other than by the ("vertical") transmission of DNA from parent to offspring. HGT is an important factor in the evolution of many organisms....
  Most thinking in genetics has focused upon vertical transfer, but horizontal gene transfer is important, and among single-celled organisms is perhaps the dominant form of genetic transfer.

--From Horizontal Gene Transfer Wikipedia page
So yes, it seems as if the fungi that you mentioned and other similar types of fungi would be strictly unicellular, such as yeast (thought yeast is a facultative anaerobe).

It is well known that anaerobic breakdown of glucose produces 2 molecules of ATP per molecule of glucose. It is also well known (see, for example, here) that fully oxidizing it to carbon dioxide and water (obviously, an oxygen-dependent process) adds up to a net energetic benefit of an additional 36 molecules of ATP. This is a massive difference. In an oxygen rich environment, anaerobes would be vastly outcompeted by aerobes, simply due to the vastly greater energy budget of the latter. As for anaerobic environments, complex (as in multicellular) anaerobes are still not prevalent, not because they are being outcompeted by aerobes, but because complex organs and systems require a lot of energy to maintain an function, energy that anaerobic respiration can't provide. Obviously, the energy requirements increase with an organism's size and complexity - the farther cells are apart, the more energy it takes for a signal to be sent in between them, e.g. via a signal peptide/protein or a hormone through a vascular system that requires energy to function, a nerve impulse, etc. Conversely, unicellular organisms avoid the energetic costs of intercellular signaling altogether (there are a few exceptions here and there, e.g. colony-forming microorganisms, but these expend far less energy on communication than cells in multicellular organisms). Numerous very interesting works on the energetics of cells and organisms are available - see, for example, here, here, and here.
One may point out that glucose, although the predominant source of energy for cellular metabolism, is not the only source, inorganic compounds from thermal vents being the alternatives most often cited. However, these are far less energy dense, with ecosystems centered around them being far less dense and complex than the ones centered on sun light and photosynthesis (Orcutt et al., 2011). Interestingly, even is such deep sea systems, the predominant source of energy is often the organic matter sinking from the photosynthetic ecosystems above.

Oxygen is by far the most common oxidizer (hence the name!) in biology on Earth.

Nevertheless, aerobic respiration provides more energy out of a unit of substrate than anaerobic respiration. Hence, where ever aerobic respiration is possible, aerobes are far more prevalent than anaerobes.

Also, you cannot fully oxidize an organic molecule simply by dehydrogenetation, to get all the chemical energy out of it you need an electron acceptor (most commonly oxygen); that applies to all organic compounds, glucose was just an example.

One must wonder if there was an abundance of multi-cellular anaerobes that existed before the Great Oxygenation Event (2.45Ga), but were never recorded (or discovered yet) in the fossil record.
The wikipedia article also suggests that ancient anerobes, before the Great Oxygenation Event, may have had more nickel to work with: "Modern methanogens require nickel as an enzyme cofactor. As the Earth's crust cooled and the supply of volcanic nickel dwindled, oxygen-producing algae began to out-perform methane producers, and the oxygen percentage of the atmosphere steadily increased.[23] From 2.7 to 2.4 billion years ago, the rate of deposition of nickel declined steadily from a level 400 times today's."

What is the connection between nickel and uni-/multi-cellularity? The first part of your answer fits best as a comment. It does not really attempt to explain why there aren't multicellular anaerobes

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Finding targets of transcription factors
I'm trying to find an easy way to get a list of putative targets of a particular transcription factor (for example, STAT1). I'm interested in targets determined using both experimental and computational evidence. I thought it should be easy to obtain such a list, but I'm having a hard time. Could anyone help me with this, preferably with specific, step-by-step instructions. As a bonus, I'm also interested in the reverse problem, which is, for a given gene, obtain a list of all transcription factors for which there is evidence that it regulates that gene.
Thanks,
Jennifer

If you were interested in human targets, one easy way is GeneCards, which aggregates other resources, and combines computational and (some) experimental data:
In this case the inverse problem is particularly well accessible: e.g.: scroll down to section of Genomics (e.g.: for the gene called NOTCH http://www.genecards.org/cgi-bin/carddisp.pl?gene=NOTCH1&keywords=notch1 ).
If you you were interested in obtaining all genes of a given transcription factor, you could buy a license, costing around 150 USD per year, for the GeneALaCart service of the company that runs the free genecards ( https://genealacart.genecards.org ), upload a list of all human genes (which you could for instance obtain from ncbi's ftp server), and get a spreadsheet linking transcription factors to genes.


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Why is the number of cells virtually a constant?
Going back to highschool, I learnt about mitosis: in order to renew their cells, eucaryots' cells divide themselves into two copies.
But my course didn't cover what moderate the replication. By moderation, I mean something that prevent the number of cells to grow forever.
So here is my question:
What phenomena are responsible for the moderation of cell replications?
I did some research on my own on both the internet and SE, but couldn't find anything (maybe because I don't know the correct keywords)

You want to try googling 'cell cycle control' - perhaps also in the context of cancer.

You have to understand this is a very, very, very, very broad question. Decades of research in multiple disciplines allow us to answer this question in a million directions. However, I would start by looking up information about the cell cycle and its checkpoints. Here of course I would point you - for starters - to this page:
Khan Academy's page on cell cycle checkpoints
For further reading, you can consult the college-level chapter on Cell communication and cell cycle regulation. Here the most relevant section would be Regulation of cell cycle, it's a great introductory read, well researched and well presented didactically.
A short tl;dr
In short, cells have checkpoints at different stages of their life cycle - both before and after they divide. You can imagine that, for instance, a nutrient starved cell incapable of copying its DNA prior to division, will arrest its progress through the cell cycle at the checkpoint before S (DNA synthesis) phase. And under the right conditions, it will resume its progress and get ready for division. This example is only one of many checkpoints that exist, and varying types of cells may have varying checkpoint requirements.

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Sexual devolpment and sexual organs in humans
In an anatomy book from a friend studying medicine (Netter's book), I looked at some elements of sexual development in embryos. From a developmental stance, we can draw some analogous organs that correspond to the same organ earlier in development:
For example:

Clitoris <=> Penis
Scrotum <=> Vulva

In this book, there is not much more. Yet, I was wondering whether we could find the counterpart of any organs in the reproductive systems of each sex. There wasn't for example any counterpart described in this book for vagina in males, or for prostate in females.
Has someone any reference to give that list the most counterpart we can find between both sexes?

Have you looked at this answer to a related post?


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Optimal agriculture: maximum yield with minimum environmental impact
I read more and more stuff about alternative method of agriculture such as permaculture. Howerver, I'm not an ecologist or biologist so I don't know where to look for really good and serious articles / paper on the subject. I am really interested in food production methods that may be efficient and respectful for both the environment and the health.
The question that interests me the most is the question of crop yield and environment. I wonder if there are studies that compares the crop yield of the different production methods AND if there are scientific researches on the optimisation of the food production under ressources constrains.
Do you have any reading suggestion? I'm mostly interested in scientific papers but I'm open to anything that may be interesting.

Google Scholar is often a good place to start your searches. Start big (broad topics, review papers), and work your way into more specific topics as you learn how different terms are used in scientific publishing. You may not be able to access certain (probably most) literature without institutional credentials, but you should at least get to a summary/abstract page, and you can always try SciHub for the full text (I'll let you figure out how that one works).

Publications by the Food and Agriculture Organization http://www.fao.org/documents/card/en/c/ca9692en of the United Nations would be a good place to start as they are freely accessible. There are plenty of articles looking at crop yield of different production methods and different management techniques. You may consider subscribing to a journal, like Agronomy https://www.agronomy-journal.org/, or CAB Abstracts https://www.cabi.org/publishing-products/cab-abstracts/ as those would contain most of the subject material you're looking for. Those would also contain information on optimizing food production under resource constraints. Happy researching!

Welcome and thanks for your post. Can you add links to websites or add other linked resources in your answer to enable other users to check out your suggestions more easily?

I believe you are looking for information on "sustainable agriculture". There are many aspects of production in agriculture like: fertilization, irrigation, pesticides and (no-)tillage. One can try to calculate the carbon foot-print of food (beware of the calculations, they might be misleading).
Crop rotation is helpful in sustainable agriculture but it is not always available, making  traditional (industrialized) agriculture the only viable option. The economic aspect is also important. Agricultures need to grow the food and they will grow it only if the make money from it. Organic and sustainable agricultural products get a premium for being cultivated that way but these premia go down as more farmers use them.
The question "How the yield is affected by the agricultural method" is a broad question that attract interest in research. We need to break it down to: What is yield (biomass? marketable product?) and what is agricultural method.
A great study conducted in Ontario, Canada by Stonehouse et al, 1996 compares the herbicide treatments in 3 types of farms: conventional, reduced input and organic and the yield, investment and profit for three crops: grain corn, beans and cereal grains. The data arrives from self-reported data by the farms. This is not a fully randomized experiment and there are many differences between farms (size, investment, land) but precautions were taken to reduce them. Reduce input farmers used less herbicides than the conventional ones.
This is the table from the article

There reported more information as profitability but since this study is from 25 years ago I believe it is no longer relevant.
This study is only one showing the complexity of the subject and one of the methodologies employed. One can write various books about the subject so I hope this post gives you the direction that you needed


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Immune response to shock
I am studying nursing and have a question regarding the physiological response to shock (decreased perfusion).  In lecture notes supplied by the lecturer, he indicates that there is a neural, hormonal and immune response to shock that is compensatory.
The neural component is the activation of the sympathetic nervous system, and hormonal response is through RAAS, etc.  This makes sense, as these mechanisms attempt to increase blood pressure and blood volume
I don't understand the immune response, though, which is described as the release of pro-inflammatory mediators, which lead to endothelial cell damage, making the vessels leaky, leading to oedema.  So how is the compensatory, it seems disruptive?  And why exactly would pro-inflammatory mediators be released in response to shock in the first place?

While I'll try to flesh out an answer when I can, try to access this article. There are some fair points, but importantly that tissues release inflammatory mediators in response to damage and stress.

Also this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846925/

Great articles, thanks.  I think this basically fills the gap in my knowledge.  So ischaemia from any form of shock causes endothelial damage, which leads to inflammation, etc...

First: what is inflammation.  From wikipedia
https://en.wikipedia.org/wiki/Inflammation

Acute inflammation is the initial response of the body to harmful
  stimuli and is achieved by the increased movement of plasma and
  leukocytes (especially granulocytes) from the blood into the injured
  tissues. A series of biochemical events propagates and matures the
  inflammatory response, involving the local vascular system, the immune
  system, and various cells within the injured tissue.

Second re shock: why does it happen?  If I go into shock from blood loss after a terrible knife juggling accident I will probably not have the inflammatory piece: I am dying from lack of blood and consequent low blood pressure.
What if I am in septic shock?  That means shock caused by organisms, usually bacteria, in the blood stream.  Bacteria are the ancient enemy and we have layers upon layer of defense accumulated over evolutionary time.  The reason we have them is that somehow, our ancestors that had them had some fitness advantage - probably because they survived having bacteria in the blood.
Some of the stuff that comes with that package does not seem very adaptive - like the leaky vessels and lungs filling up with fluid.  Maybe we see the wild extreme of this reaction but to a lesser degree (lesser infections?) those inflammatory responses are good?  Maybe releasing a storm of neutrophils has unavoidable side effects for the surroundings - like the Avengers fighting an alien army in NYC?  It was tough on NYC.  Maybe those extreme shock reactions save the organism 1 time in 10, which is better than the odds otherwise with an overwhelming bacterial infection.
Bottom line though is that bacteria in the blood in great numbers is an existential threat to the organism.  Desperate times call for desperate measures.


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How is chloride concentrated in nerve cells?
Bear, Connors and Paradiso describe in depth the electrical behaviour of the neuron. This depends upon a 20:1 concentration within the cytoplasm of potassium ions AND chloride ions. All subsequent activity revolves around potassium and sodium ion channels and pumps. No mention is given of how the initial chloride concentration is created and its subsequent regulation. Obviously there has to be a chloride pump but there’s no mention of it. Any help would be appreciated.

Check out the potassium-chloride cotransporter KCC2 as well as GABA Receptors as chloride ion conductances in neurons.  Maybe overkill but a nice review here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4294553/

Many thanks Louis. I’m a beginner in cell biology and perhaps I misread the diagrams in Neuroscience exploring the Brain. It makes sense to me now just to assume that the neuron gains its anions soley from those provided by the ‘original’ dissolved potassium and sodium salts that were isolated within the cytoplasm during the cell’s devolment. Perhaps I’ve got it right!

Not quite, the examples I listed show the neuron has capabilities to change its internal anion concentration (passively or actively) which has knock-on effects for it's excitability and is not just what is left over from the ionisation of salts containing chloride.  Hope that makes sense.

Wow! The abstract gets you going, eh Louis?! Thank you so much. I’ll be reading all 43 pages. Best wishes Mike Kidd.

Thanks to Louis Leung introducing me to cellular cotransportation I can now envisage how the neuron (in particular) obtains its “background” chloride base thus enabling thecreation and transmission of nerve signals. Given the presence of sodium-potassium pumps and NKCC1 sodium-chloride cotransporters we now have a mechanism for achieving the necessary chlorode base negativity in the neuron’s axon. I’m sure that Louis will correct my amateurish description if it’s in serious conflict with the science!

I think you are doing just fine @adlibber! Just be sure to keep the chloride role in action potential propagation in context since for APs, the dominant ion conductances are still Na+, K+ and Ca2+ since the reversal potential for chloride exchange is generally close to the resting potential of neurons.  If that review was still not enough to satisfy you - I think this one may be even more suitable: http://www.sciencedirect.com/science/article/pii/B9780123877383000159

My poor brain Louis, but once again I thank you!


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Why is there a distinction between an *allergic* and an *immune* response?
Our immune system has evolved to protect us against potentially dangerous non-self particles. I have difficulty in understanding why there is a distinction called an allergic response: what’s wrong with using the term immune response full stop? Surely a person’s immune system should react to a particle of grass pollen in EXACTLY the same way as it does to a non-self protein expressed on cells of some transfused blood. The mystery that I absolutely don’t understand is why our body can then differentiate the scale of the response.

Doesn't an allergic response involve completely different mechanisms from immune responses?  Certainly at a high level we see much different effects, e.g. allergies involve histamines so we treat them with anti-histamines, while immune responses involve fevers & white blood cell production.

Have you found a satisfying response? I am curious of how difficult it is to find information on this, and this being the only question our of 2 in stack overflow asking this

The trouble is, you can't live without being exposed to all sorts of non-self particles. Some of those particles signal an actual threat to your health (proteins associated with a disease causing virus), some are nearly harmless (bee stings), some are completely harmless (grass pollen or cat dander), and some are potentially valuable as part of a food substance (seafood or peanuts). Ideally you'd like your immune system to respond to the harmful ones, and ignore the harmless or useful ones. An allergy is defined as an unneccesary immune response to a harmless (or nearly harmless) substance.
You do want your immune system to deactivate venom from a bee sting, but you don't want it to react so strongly that as a side effect your throat swells up and you can't breathe. Most people breath in grass pollen every day of their live with no ill effects, so those folks who have an allergy to grass pollen are being made miserable by their immune system to no good purpose.
Ideally the immune system mounts a full response only when the presence of particular non-self particles is associated with other signals indicating that something "bad" is happening which merits an immune response. However, the process by which the immune system is regulated is incredibly complex, involving feedback loops from hundreds of different chemical pathways and dozens of different cell types. The process is imperfect. Sometimes it goes wrong, and the immune system mounts an aggressive response to a harmless foreign substance or even worse part of your own body.

Thanks, Charles. That’s an interesting point you make that our immune system can somehow associate a non-self particle with any damage it causes (prior to any immune system mediated damage).

"An allergy is defined as an unneccesary immune response to a harmless (or nearly harmless) substance.". The problem here is that the immune response also seems to be different in the case of exposure to an allergen and a pathogen, which as OP points out, implies the body is "aware" one is harmful and the other is not..

Allergy is an exacerbated inflammatory reaction of the immune system in reaction to small quantities of foreign inert substances called allergens. It is a clinical condition characterized by its symptoms: redness of the eyes, ocular and nasal discharge, itching, eczema, asthma, headache, digestive disorders and swelling.
The most critical clinical manifestation is the anaphylactic shock that may lead to death.
The immune reaction is triggered by pathogens (viruses, bacteria, parasites) that have the ability to replicate within the body.
Both the allergy and the normal immune reaction share the same principle: a primary immune response where the immune system learn about the antigen/allergen, and a secondary immune response where it can unleash its full potential (too much in the case of allergy).


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glycogenesis, glycogenolysis and weight gain or loss
I am under the impression (from dietary websites) that when excess serum glucose is stored as glycogen, body weight is increased and the reverse: when glycogen is converted to serum glucose, body weight is reduced.
I also understand that the glycosidic bond formation in glycogenesis is a condensation reaction, releasing water, whereas the rupturing of these bonds in glycogenolysis is a hydrolysis reaction absorbing water.
Please help me here: how does the body gain weight by releasing water and lose weight by absorbing water. What am I not understanding?

shat happens to the sugar in blood stream?

Where I say ‘serum glucose’ I really mean ‘blood glucose’. Apologies.

sure, whatever. My point,  if you answer my question, you'll be able to get more intuition into your question

You ask about what happens to sugar in the bloodstream, I presume you mean glucose in the bloodstream and, if you don't know the answer to your own question, I don't think you're going to be able to help me. Sorry!

i am trying to give you a hint. If you can answer what happens to glucose in blood stream, you might be able to understand how weight loss works

Well, aaaaa, I thought I knew, but perhaps I’m missing the obvious! Please help my seventy-six year old brain, befuddled with glycolysis, Krebb’s, ketones, gluconeogenesis and heaven knows what else to get to the bottom of my question!

A point of significance - main energy storing component is fat and not glycogen. A 40 minutes - 50 minutes moderate to severe exercise is sufficient to clear up most glycogen in the body. Thus the contribution of glycogen to body weight is very insignificant if any

One face, many thanks for your comment. Many tests have shown that shortly after starting a LCHF diet there is rapid loss of up to 5 kg. For me it took about five days. The only plausible explanation is the consumption of glycogen stores, see my self-answer below. As you know, fat is hydrophobicand so no water weight is lost due to fatty-acid oxidation.

The answer to my question is that the glycogen molecule is extremely hydrophilic. For every gram of glycogen the molecule attracts 3 grams of water. When the glycogen is hydrolysed the attached water is excreted either directly in the liver or through cellular ATP processes.

you should provide links to deference where you got this information

I found this out studying the excellent biochemistry series at the Khan Academy.

I think your trouble comes from incomplete understanding of glucose life in the human body. Basically, you need to look at Citric Acid Cycle or TCA, that works with Acetyl-CoA as starting compound.
The reaction can be condensed into:

Products of the first turn of the cycle are one GTP (or ATP), three NADH, one QH2and two CO2

The weight loss that you are interested in, comes from basically releasing CO2 into the air. As far as I understand, you breath your weight away! Interestingly, trees are going to use that CO2 later to build their tissues up.
The water doesn't play central role in process of weight loss, as body tries very hard to regulate amount of water inside the cell and in the intracellular space.

I have an answer to my problem and it is thanks to Khan Academy. Of course it is SO SIMPLE!

your source is undoubtably correct regarding fat burning aaaaa, not only carbon dioxide of course but also water are the end products of cellular respiration. But that wasn’t my question which concerns the rapid weight loss experienced by folk starting a Keto Diet.


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Understanding transplant rejection - how does the cellular, adaptive, response get underway
This lay person is trying to get his head around the basic mechanisms of tissue rejection.
A lot of articles talk about T-cells being involve but I'm having difficulty following this. Human tissue is essentially similar between individuals. As I understand it the only cellular membrane protein that is (almost) unique is the major histocompatibility complex (MHC) that is expressed on all nucleated cells.
This means that killer T-cells can't recognise transplant tissue cells because of the MHC mismatch. The only cells that can identify non-self human tissue are the humoral innate immune natural killer cells (NKC) and they do this because they are built to kill anything unless it displays self MHC.
OK so NKC spew out the remains of alien tissue cells, but these residues are surely very similar to any other self cells' internals? How do I move from this view to one that involves the adaptive immune system which requires presentation of cellular fragments to lymphocytes?

I have just read some recent paper on the interaction between NKCs and dendritic cells (DCs). This would provide a way of activating the adaptive immune system providing the DCs were able to present some non-self material from the digested donor tissue. But apart from MHC what differentiating material is available from a donor tissue cell?

Please add reference, link. I think you're on the right track, as there  is spectrum of cell types ranging from NK to Tc-cells.  Your question refers to identical antigens being presented by self APCs? Even if T cells specific for that "identical" antigen (it's "common tissue", no MHC allo-forms) were "cross-reactive" to allo-MHC -- they would not exist any more as they had received "death signal"...

There's a really good paper on this, Moreau et al., worth reading through entirely. The only caveat is it was published in 2013, so as a rapidly evolving field such as immunology we might have more insight now. However, the general concepts remain the same.
The lymphocyte compartment that we generate in our own bodies is modulated so that it isn't autoreactive. In other words, for every antigen a T cell should expect to actually encounter in vivo, the ones that attack and kill self cells are made to undergo apoptosis, the special case of course being autoimmunity, which is a set of diseases.
An organ transplant is what's known as a so-called allograft. The allo- prefix implies that the origin is the same species, but from different individuals. So how do people differ at the molecular level? Well for one, we inherit and develop slight differences to such things as protein sequences, carbohydrate chain moieties, and certain receptor combinations. So, your lymphocyte compartment may be non-autoreactive, but it could be alloreactive because those aren't your signals.
The other thing transplants do is cause damage and inflammation that result in the presence of these patterns that the innate immune system respond to called PAMPs and DAMPs, or molecular patterns associated with pathogens and tissue damage. They also bring along donor immune cells like antigen-presenting cells, resident lymphocytes, granulocytes, etc. It's also a functioning tissue, and so just like any of your own cells, a liver cell is expressing class-I HLA loaded with alloantigens. This can have two effects: graft-versus-host, so you have donor immune cells attacking the recipient, and the rejection which is where your recipient immune cells attack the transplant.
Your immune cells attack the transplant predicated on direct and indirect recognition, and the fact that all that inflammation already has the immune system up in arms. So your lymphocytes recognize an alloantigen on the donor antigen-presenting cell is an example of direct recognition. This can occur in the transplant, and also in the recipient lymph nodes as donor APCs can traffic there on signals in the lymph. Recipient APCs can also pick up on alloantigens from donor cells and active the adaptive immune response classically, which would be an indirect recognition.
The blanket treatment for this seems to be immunosuppressive therapy.

Many thanks for the response. I get the point re donor antigen rejection but you also mention "your lymphocytes recognize an alloantigen on the donor antigen-presenting cell". My understanding is that recognition can only be achieved when the antigen is presented on self MHC type I protein. According to current thinking killer T-cells will ignore any antigen presented on non-self MHC. This difficulty (perhaps my understanding) is at the heart of my question.  I am referring to donor tissue cell rejection here rather than any other donor cellular type. NKCs will do the job of course!

@adlibber That's a good question on it's own. Here's a fairly recent paper that attempts to expain direct allorecognition: What Is Direct Allorecognition?. What you'll find out, in part, is that's it's own long answer and I'm less informed about that topic.

I think I got from the Direct Allorecognition paper the fact that the differences between donor & recipient MHC II is unimportant during donor dendritic activation of host T cells. If my understanding is correct then when the T cells are presented with donor MHC I fragments the adaptive response is activated. Very interesting re MHC II not being an issue.

The question says: "Human tissue is essentially similar between individuals." The answer says: "we inherit and develop slight differences to such things as protein sequences,..." Would be helpful to have some quick reference to textbook on allo-antigens. Anyway, the question's focus is on antigens being identical on cells that differ in their MHC.

Your question refers to the problem of "alloreactivity of lymphocytes".
There are several related questions on stackexchange, and there is plethora of literature, some call it puzzle, enigma; your question is valid.
You emphasize twice that  MHCs of host and graft are different whereas antigens are  identical (as graft and host are no different species):
"Human tissue is essentially similar between individuals. (...) the only cellular membrane protein that is (almost) unique is the major histocompatibility complex (...). And: "OK so NKC spew out the remains of alien tissue cells, but these residues are surely very similar to any other self cells' internals?" (only in your comments you mention that non self MHC as a "surely not similar" antigen may be presented on self MHC (which it is is fact, by the way))
What is the implication of antigens, contrary to MHC, being the same?
That there has been undergone a process of tolerization, of sorting out, of "negative selection" of T- and B-cells that are specific for that same antigen of host and graft.
Quote:  "My understanding is that recognition can only be achieved when the antigen is presented on self MHC type I protein. (...) This difficulty (perhaps my understanding) is at the heart of my question. (...) NKCs will do the job of course!"
I believe what you imply is that any T cell that might attack its specific antigen on non self MHC would have been sorted out by negative selection: no one left to present the antigen to on self MHC, the ones have been departed or gone.
How can any T cell escape "negative selection" if it is specific to the same, identical antigen which after transplantation is presented  on foreign or self cell, be it by APC cell or tissue cell. Any T cell specific for that antigen should have received a "death signal" and not exist any more. I think that is "at the heart" of your question.
Can "cross reactivity" (see literature)  solve the problem? This is difficult to see if you have that paradox of  "sorted out" in your mind. There seems no T cell "left " to attribute that quality to.
However, there is  "tolerance". Any basic textbook will not elaborate on Lymphocytes specific for the antigen being NOT sorted out. They do exist. In "negative selection" only lymphcytes that bind too strongly receive a death signal, there does exist a set of T cells specific for that antigen that are "tolerant", weakly binding, and escape to the periphery.  I think it is a possibility that they act "crossreactively" when that same antigen is being presented on foreign MHC (as they may bind "strongly" to foreign MHC, to explain: if they had been negatively selected by foreign MHC they would have been sorted out as "too aggressive", assuming they bind strongly to foreign, allo-MHC, weakly to self, iso-MHC), and, when being activated by APCs presenting that antigen, which might be host or graft MHC.
So I will carefully reread my textbooks, and these are a few learner's hints added: in positive selection, there is "already" specific peptide, antigen, being presented. If you see the antigen in positive selection that is not a process of killing any cell that does not bind to self MHC, in other words their might be a set of lymphocytes that do not bind strongly enough "in the first place" and do not enter positive selection as they "only" bind graft MHC. Second hint: the death signal in negative selection goes to the self MHC binding cell (just the opposite). The set described above leaving negative selection may very well be  the one which is said to be "cross-reactive" in literature).
The gist: First, it is not true that there is "positive selection" that does not present (self) antigen. Thus, it is not true that in positive selection all lymphocytes that do not bind self MHC are sorted out and eliminated. "They came for the antigen", that is my hint.
Second, refering to negative selection: it is not true that any lymphocyte is sorted out that binds to self antigen. The ones that might bind that specific antigen but do not bind too strongly, do not become aggressive with "their" self MHC "leave laughing". Logically, they might bind strongly with  that specific antigen plus NON-self MHC. Non-binding strongly with antigen plus self-MHC does not imply non-binding with transplant-MHC plus antigen.
Hint: it took me a long time to put it that easy.


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Do DNA footprints vanish in generations?
Consider humans (or really any creature with sufficiently complex set of genes).  If person $A_0$ has an offspring, say $A_1$, we can without a doubt find markers in $A_1$ that we can definitely say indicate that $A_1$ is the progeny of $A_0$.  Likewise, for any generation $n$ we can say that $A_{n+1}$ has markers that indicate that generation $A_n$ is their parent.  Presumably (and maybe this is where I'm heavily mistaken), as $n$ grows large there are fewer "direct signs" that $A_n$ has $A_0$ in their ancestry.  I mention "direct signs" (although this isn't an official term) because obviously if one can prove $A_{n-1}$ is the parent generation to $A_n$ and $A_{n-2}$ proceeds $A_{n-1}$ and so on ... then one can deduce the relation between $A_0$ and $A_n$.  That's not my point.  My question is this:  Do the genes of $A_0$ "dilute" so that after so many generations it is possible or probable that none of the genes from $A_0$ are present in $A_n$ for some large $n$ (where by "none" I mean "no genes that give us a high warrant for believing $A_n$ is related to $A_0$ in the absence of evidence about $A_j$ for $2\le j \le n-1$").  Obviously if $A_0$ is human and $A_n$ is human then they share a great deal of their genes with one another (something like $99.99\%$)
If there is such an $n$, how large does $n$ need to be so that say $90\%$ of what makes $A_0$ unique is no longer present in $A_n$ (with a high probability of confidence), what about $95\%$ no longer being present, or $99\%?$
Please let me know if my question isn't sufficiently clear (I'm trying to convey the heart of my question, even if it isn't perfectly worded).

You seem to be figuring that since $A_1$ has half the genes of $A_0$, and $A_2$ has half the genes of $A_1$, etc throughout the generations, we quickly get to a point where $A_n$ has none of the genes $A_0$ had.
This would be correct, if we assumed no inbreeding among the descendants. And by "inbreeding" I don't mean siblings or first-degree cousins breeding, but any of $A_0$'s $n^{th}$ descendants breeding with another. Which is clearly absurd; at some point you're going to run out of breeding partners who aren't also a descendant of $A_0$, unless the lineage isn't very prolific and the number of descendants $A_0$ has is always a small proportion of the total population. And in that case, sure, those genes are probably going extinct.
The same thing happens the other way around by the way; we (most of us) have two grandparents, four great-grandparents, etc. As we go back in time this exponential growth quickly outstrips the amount of humans that were alive at the time our $n^{th}$ great-grandparents were around. That's because that exponential growth assumes no inbreeding, which there is. There is a point in time in the past beyond which everybody alive today is the descendant of everybody back then who has any descendant at all; that's called the Identical Ancestors Point. See for example:
https://www.nature.com/news/2004/040929/full/news040927-10.html
The end result is that there are really two outcomes for $A_0$'s descendance: either they increase over the long term faster that the overall population grows, or they increase at the same rate or slower. In the first case, we'll reach a point where the whole population is part of $A_0$'s descendance. In the second, unless population growth is huge then $A_0$'s line is probably going extinct. Even if not, and if we assume individuals are breeding randomly throughout the population (not a good assumption, but no gene dilution without it), then the original assumption that $A_0$'s descendants have fewer and fewer of $A_0$'s genes every generation is correct, and $A_0$'s genes will likely go extinct even if their descendants don't.
On the other hand if $A_0$'s descendance end up consisting of the whole population, then no more "dilution" can occur. Say at that point every individual has 1% of $A_0$'s alleles; their offspring will also have 1% of $A_0$'s alleles on average, and same goes for all later generations.
Note that at that point $A_0$'s alleles are distributed throughout the population; even if everyone has 1% of them, they don't all have the same 1%. So the question of whether "what makes $A_0$ unique" is present in the descendants is really hard to interpret. Some of $A_0$'s alleles may be present in everybody at that point (they have become fixed in the population), some may be present in X% of the population, some may have gone extinct. The specific combination of alleles that made $A_0$ is gone, but then it was gone when $A_0$ died. As for the question of whether scientists can investigate the descendants and find traces of $A_0$ after all those generations, the answer is "sure": see the aforelinkedto nature article.
More to the point, consider this sentence you wrote:

Obviously if $A_0$ is human and $A_n$ is human then they share a great deal of their genes with one another (something like $99.99\%$)

Do you not see how this factoid relates to your question? You are asking whether human $A_n$ still shares some genes with its ancestor human $A_0$, and caveat that "obviously" they already share most of their genes, what with being human. You mean, what with both descending from the common ancestor to all humans. That those $99.99\%$ of identical genes come from. Except of course that not even, given $99.99\%$ of that $99.99\%$ comes from our common ancestors with chimpanzees, and so on. Most of "what made the common ancestor to all life unique" is still in our genes today! So yeah, it will take more than a human-scale $n$ generations for all traces of a human ancestor to be predictably erased from its human descendants (keyword "predictably"; in practice many lineages and alleles do go extinct, but not all do and you can't really tell which in advance). More than that, on those evolutionary timescales natural selection is a strong force and you get phenomena like conserved genes - that is, genes that are important to the organism and are thus selected for to stay the same. At that point there is no "random dilution" phenomenon happening: there are specific forces at work to maintain the gene in all descendants in a more-or-less unchanged state.

We can reconstruct the pretty much the entire tree of life from genetic data! Of course, the further you go, the harder it becomes to know the exact relationship between individuals.
The false concept of gene dilution
I think most of your misunderstanding comes from the idea that genes "dilute". Genes are particular. An allele  (=gene variant) is either transmitted or it is not. But it is not like it would be a little bit transmitted. Consider the classical (historically important and obviously racist) "bad" argument of Jenkins

Jenkins supposed that a white man was wrecked on a desert island inhabited by Africans. The shipwrecked European would kill many black men in struggle for existence. He would have many wives and children. Many of his subjects would live and die as bachelors. In the F1, there will be some intelligent young men who are mulattoes (mixed race) more intelligent than negroes. Eventually instead of the beneficial white characteristic rising in frequency through natural selection acting on intermediates, Jenkins said that the European alleles and genes will be diluted out.

Putting aside the obviously racist and false assumption that whites are superior to blacks (such extreme racism was standard at that time in England), the argument does not sound so silly. Why would not the beneficial characteristic of an individual just dilute into the majority unadapted population? This concept was called blending inheritence and was the major way of thinking during the 19th century until the rediscovery of Gregor Mendel's work.
Individual characteristics are not 'fluid'. Characteristic of parent don't just average to give the characteristic of the offspring. There are actually particular unit of heredity (a gene) which has some 'atomic' property in the sense that it will be transmitted or it will not but nothing in between.

Assuming no inbreeding, you have 4 grandparents, 8 great-great grandparents, 16 great-great-great grandparents, 32 great-great-great-great grandparents, 64 great-great-great-great-great grandparents.
So sure, 98.4% of your genome came from someone other than that one great-great-great-great-great grandparent.  And most of that 1.5% is shared by every single person.  If that 1.5% doesn't contain any mutations unique to that ancestor, then sure, I guess it's lost.


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What is it called when an animal only has one type/variation of dentition?
An example would be alligators that only have one type/shape of tooth. Not the variation in function and shape like seen in humans, which have canines, molars, incisors, etc

Homodont
You can find the term "homodont" used in Lambert et al. (2014) or on wikipedia > dentition for examples. The opposite of homodont is heterodont (wikipedia > heterodont). In mammals, a classical example of homodonts is the dolphin.

to reinforce heterodont dentition is fairly rare, only mammals with their limited number of teeth have it constantly across a large clade.


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What are the issues with excessive tandem repeats in replication?
Why is it that tandem repeats like CAGCAGCAG cause primer-template misalignment and diseases like Huntingtons disease? By my understanding, too many such repeats can cause strands to form hairpins and loops that fail to be replicated in the template strand, causing deletions. Is this correct?

What research (see Help) have you done to try to find the answer to this question yourself? You should be able to find it very easily on the internet.

Moreover, your question is unclear. Are you asking how these repeats increase or how they cause disease?


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Michaelis Menten kinetics - Plotting to find V-max and Km
In dealing with the question above I know that if we plot 1/v against 1/[isocitrate] we can get V-max = 1/intercept and Km = slope/intercept.
However when I express the two rows of values in micromoles I get intercept = 3359, and I believe it will be in micromoles? That gives me V-max = 1/(3359*10^-6) = 297.7. However, how do I know the order of magnitude of this number? The textbook says it is pmol, but how is it picomoles/ dm3 s?

I'm voting to close this question as off-topic because this is not about Biology but numerical manipulation, and in a specific instance. There are many resources on the web for this sort of thing.

Another more general point. Do not post text as images. It discriminates against people with sight disabilities.

The order of magnitude for your intercept value depends on the axis of your graph, which in turn depends on the values / units of your input values.
As an example if your substrate concentrations are in the range of $\mu mol / l$ (which is micromolar, not mircomoles), then that is also the order of magnitue you'll get out of the calculation.
$dm^{-3}$ equals litre's ($1dm^{-3} = 1l$), it's not usually not used for concentartions, so I can't say why the textbook used it instead. Maybe they wanted to use base SI units.


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Why does resting potential not become continually more negative?
(Firstly, I know this is similar to other questions, but I have read those answers and they do not really cover this topic).
My understanding of resting potential: action potential is not being transmitted; by way of action potentials via Na+ and K+ pumps, for every 2K+ pumped in, 3Na+ is pumped out of the cell. This process is termed "resting potential" and the transmembrane pd roughly = -65mV.
If more Na+ are pumped out than K+ in, why does the resting potential difference remain at -65, why does it not continue to decrease (until an action potential is triggered)?

The resting membrane potential is due to internal/external differences in ion concentrations and very importantly differences in permeability to those ions.
The fact that the sodium/potassium pump does not move an equal number of ions in each direction hardly matters at all for resting membrane potential; the resting membrane potential would be almost the same if that wasn't true. What is important is just the overall concentration of the two ion species, and the permeability of the membrane to different ions (almost all of this permeability is through specialized ion channels, because ions don't otherwise flow easily through a lipid bilayer).
You can calculate the resting potential/equilibrium potential using the Goldman equation - note that nothing in this equation involves the sodium/potassium pump moving different numbers of sodium and potassium ions.
The reason the membrane potential is negative is because the membrane at rest is most permeable to potassium, and because there is more potassium inside the cell than outside. Therefore, there will be a net flow of positive ions out of the cell, until enough ions have left that there is some negative charge inside the cell to counteract that net flow.

As you mentioned, the pump will keep generating an ionic gradient (and the membrane voltage should decrease)
Nonetheless there is still open ion channels at these negative potentials. Then the resting potential will be the voltage at which the net ion Flux (ion channels + leak + pump) is zero.
Since the pump is electrogenic (generates a current) the standard Goldman equation is not applicable and has to be modified.

Here $I_{pump}$ is the current generated by the pump. This equation can also be applied when other electrogenic pumps or transporter are present
You can see the derivation in this paper.

This answer is a bit misleading, the resting potential is almost entirely due to the differences in permeability, only a couple mV has anything to do with net flux through pumps.

@BryanKrause I expanded the answer a little bit  to show how the pump affects the membrane voltage


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How does antibody structure relate to function?
I know that antibodies have 2 binding sites (as Y shape) so they can bind to 2 pathogens for agglutination. They have a hinge, heavy and light chains, constant and variable sections on these chains.
But how do these structures (and any obvious structures I have missed) relate to the function of antibodies?

This is a broad basic question that is well covered on numerous sites on the internet as well as standard texts that an be read on NCBI bookshelf. If you read the help on "how to ask a good question" you will see that you are expected to explore such sources first. Try a search for antibody structure and function or consult Ch 33 of Berg et al.


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How does (action potential) hyper-polarisation work?
I understand that after depolarisation, repolarisation and then hyperpolarisaiton occurs and that an area in hyperpolarisation is in its "refractory period".
Why does this prevent Na+ ions diffusing "backwards"? Since an area of the neurone membrane in hyperpolarisation will have a very negative charge so surely positive Na+ ions would diffuse towards them rather than away from them - "forward".
Similarly, why does this prevent another action potential firing too soon?
(I know this is kind of 2 questions in one, but as they are so very related I thought it more prudent to combine them).

Possible duplicate of: https://biology.stackexchange.com/questions/56621/why-does-the-refractory-period-of-neurons-only-allow-signals-to-pass-in-one-dire

Yes, that answer kind of answers my first part of my question (about being uni-directional) but doesn't answer the part about another ap firing too soon. Although I see why you might think it's a duplicate :)

I'll borrow a diagram from another answer to a similar question, but not quite a duplicate (I hope @AliceD won't mind my laziness):

Fig. 1. Refractoriness. source: University of British Columbia
One important concept to understand about the refractory period is that it has two components. One is the hyperpolarizing part, which is due to open voltage-gated potassium channels. Because there is more potassium conductance than at rest, the membrane voltage gets closer to the reversal potential for potassium.
If you were to open a sodium conductance during this period, you would indeed get a larger sodium current than you would get at rest (because you are further from the sodium reversal potential), however it will also be accompanied by potassium leaving the cell (because there is more potassium conductance), such that the net current and net change in voltage may not be much larger than at rest. Voltage-gated sodium channels that open to cause an action potential are gated by voltage, not by sodium. However, this type of refractory period is referred to as a relative refractory period because you can overcome it if you open a large enough sodium conductance (or inject a bunch of current with a patch clamp amplifier).
However, there is also a second part to the refractory period, the "absolute" part, which is shown in the diagram above. The voltage gated sodium channels themselves are not only closed but they are also inactivated. While inactivated, those channels will not open even in response to depolarizing voltage. It takes some time for the channels to return to the 'closed' state where they can be opened by voltage.
Summary
To speak to your question more directly, nothing prevents sodium from diffusing 'backwards', but action potentials travel quickly, sodium channel inactivation prevents them from traveling into axon segments where the sodium channels were just recently open, and the open potassium channels that cause hyperpolarization will 'shunt' current out of the cell while they remain open. Lastly, voltage-gated sodium channels are gated by voltage, not sodium.

"or inject a bunch of current with a patch clamp amplifier" --> Current is the flow of electrons, would hence current injection not make the membrane more negative (and make it hence harder for sodium channels to open)?

@Pugl The convention is to refer to positive charge as positive current. In neuroscience, it is not in fact electrons that are moving but ions of positive or negative charge. You can hyperpolarize or depolarize a cell freely when you have access to a cell via patch clamp, it doesn't matter what is flowing in the circuit of the amplifier.

So, one would in fact inject cations (= positive current) for instance to depolarize a cell?

@Pugl Physically with an electrode it's probably more accurate to say you are attracting electrons/anions towards the cathode but it really doesn't matter mathematically.


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What is the reason behind studying seroprevalence of a disease?
Scientific literature on viral disease, specifically ones like Zika and Dengue, contains seroprevalence data. What is the reason behind understanding seroprevalence?

Seroprevalence tests people for the presence of a disease based on serologic methods. Often you do ELISA (or related methods) to test for pathogen specific antibodies.
This gives you information on how common a disease is, especially when it might infect people without them showing symptoms. It also can help detecting cross-protection when the seroprevalence is lower than expected. This is something shown in micronesia, where the seroprevalence was much lower than expected (from: Zika Virus Seroprevalence, French Polynesia, 2014–2015)

Our findings show that <50% of the population of French Polynesia had
  detectable Zika virus IgG. This seroprevalence rate is much lower than
  the 86% attack rate estimated by Kucharski et al. (14) using a model
  that assumed the French Polynesia population was 100% susceptible to
  Zika virus infection. However, in a setting where DENVs are highly
  prevalent (8), the possibility of cross-protecting immunity preventing
  infection from Zika virus (12,13) cannot be excluded. The attack rate
  and the asymptomatic:symptomatic ratio in French Polynesia were also
  lower than those described for the 2007 outbreak on Yap Island (73%
  and 4:1, respectively) (4); this finding supports the perception that
  the drivers of Zika virus transmission vary depending on geographic
  context. For other flaviviruses, such as DENV, previous model-based
  studies showed that the herd immunity threshold required to block
  viral transmission is ≈50%–85% (15). Thus, if Zika virus has the same
  epidemiologic characteristics as DENV, the seroprevalence rate of 49%
  would not be sufficient to prevent another outbreak.

It can also help to make predictions about the spreading of a disease. With a high seroprevalence epidemic spreading is unlikely, while this is pretty much different with a low prevalence. This is something which was observed in Brazil when Zika occured there first.


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Why does a distraction cause a longer reaction time?
Does it have something to do do with the fact that the individual isn't concentrating on reacting to the stimulus, so it takes longer for it to be processed? How can this be out in terms of neurones and neurological pathways? what is happening for there to be a delayed reaction time?

Do you know anything about working memory? If you want an overall explanation, the article should be sufficient (I use "working memory" in the sense of processing time, not solely incorporation of short- into long-term memory.) You're going to find it difficult to get a "what's happening on the level of individual neurons" explanation difficult.

I am not sure which sort of answer is expected. The minimal answer to that would be that the more distracted you are the longer it needs to sample the stimulus space of interest as you are sampling another distracting stimulus simultaneously with your limited sensory capabilities.
Cognitive tasks get just more complex with distraction as the brain cannot know which features (of the full stimulus space from all the sensory modalities) to take into account and therefore needs to sample more data to find out which of the inputs matter for the specific task.  In most of natural situations the inputs match together in terms of experienced stimulus combinations (visual field and sound while walking for example) except for surprising situations that require to alter ones attention (a sound that does not match to the visual scenery is unexpected and might be important to check for danger). To decide whether the system can ignore such parts of the input requires computation and computation takes time. I don't think it is useful to tackle the question in terms of delayed signaling along specific neurons or pathways. The signaling itself is more or less of constant speed and not directly altered by distraction. Of course on a very basic level an increased adrenaline level or similar due to distraction might affect the "weights" of certain basic pathways as one is pushed into another state. In such cases therefore it requires the system to compensate those changes with respect to the actual task of interest as it might be biased to different reaction scheme that is not useful for the specific task.
Actually our brains are very good in focusing on specific parts of the inputs that are important for a task (i.e. cocktail party problem) but still it needs more time to correct the erroneous parts in the presence of distraction. In terms of a simple Hopfield network that does pattern completion distraction would be like an increase of the noise level which leads to a higher number of iterations required for convergence while the speed of signal transmission from neuron to neuron was not altered.


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Chloroplasts in an animal cell
What would happen if we inject a chloroplast organelle into an animal cell?
Will the animal cell destroy it? Or is it possible that the chloroplast will somehow survive, and even replicate? Could there be photosynthesis in such a cell, or will some of the necessary mechanisms be missing?

To answer your bigger question:
Yes, most of this is possible - under some conditions -, and animals and animal cells can acquire chloroplasts, and use them.
E.g.: see Elysia chlorotica whose cells actively take up chloroplasts and use them, and keep them alive (though not replicating). - Though some genes of algae are also contained in the Elysia chlorotica genome - which may be considered as partial replication.
Also there are salamanders that have replicating algae within them (since embryogenesis) - even algae (with chloroplasts) within animal cells - though here the algae might be rather understood as symbionts or "cell types", and the animal cells don't have the chloroplasts by themselves.


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Does the mesoderm evolve from the ectoderm or the endoderm?
I know the embryos of most animals develop into 3 germ layers. However primitive animals, such as Cnidarians, only have 2 germ layers - they lack a mesoderm. Therefore the 3rd germ layer must have evolved from cells which originally differentiate to one of the two more basal germ layers.
So my question is - does the mesoderm evolve from the ectoderm or the endoderm? Meaning, during embryogenesis, which cell type is the first to differentiate from the other two - the ectoderm or the endoderm?

In human,the mesoderm doesnot develop from the endoderm or the ectoderm.It develops from epiblast of the bilaminar germ disc stage.
During the week 3 of development, the epiblast of the disc invaginate and divide rapidly to form the cells of the endoderm.The division is rapid enough to replace the hypoblast layer.
Even after the endodermal layer has formed, the epiblast continues to divide at the region of the invagination.The divided cells migrate between the epiblast(soon to be the future ectoderm) and the newly formed endoderm to form the mesoderm.
REFERENCES:

Langman's Medical Embryology (13th edition) T.W. Sadler
website

Okay. So is it correct to say that just after the endoderm develops, there are cells in the epiblast which can develop to either mesoderm cells or ectoderm cells, depending on their environment?

@Alon Navon No.Nothing is environment dependent here...its all gene regulated... either mesoderm cells or ectoderm cells  No, its genetically programmed to form both.

All the cells have the same genes. Their differentiation is dependent on various chemical signals.

There is some kind of 'family tree' between cell types. Some cells can only develop to bone or cartilage, but not nuerons. Based on this, some pair of {ectoderm, mesoderm, endoderm} is closer developmentally than the third one.

yes.true.you must have followed that the endoderm and mesoderm are formed from the cells that migrate from the epiblast...the epiblast itself forms the ectoderm...


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Linkage Disequilibrium - What does it mean when D < 0?
What does it mean when you have a situation where your D<0?

Consider two bi-allelic loci, A and B with alleles A1, A2 for A and B1, B2 for B. Negative values for D means that A1 is more often associated with B2 than expected. Similarly, A2 is more often associated with B1 than expected.
More info on Wikiedpia > Linkage Disequilibrium or on any intro book to population genetics (see here for recommendations). If there is anything in particular you do not about the definition of LD, feel free to ask a question by highlighting what is unclear to you.


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What exactly is a centimorgan?
Centimorgan's aren't physical distances. The analogy that I could come up with is if you had an array with 10 items,
A = [a, b, c, d, e, f ,g ,h ,i ,j, k]

The distance of a in the array is closer to b than k, ie A[0] is closer to A[1] than A[10] so that the centimorgan of A[0] and A[1] is less than A[0] and A[10]?

I personally like to talk in Morgan (M), instead of centiMorgan (cM), because the Morgan has a more intuitive meaning than one-hundredth of its value.
Morgan
If two loci are at distance 1M, it means the expected number of cross-over happening between these two loci is 1. If they are at 0.1M, then the expected number of crossover is 0.1. If they are at 1.4M, then the expected number of crossover is 1.4.
centiMorgan
As the typical distance of interest is much lower than the Morgan, we typically talk in centiMorgan.
Rate of recombination
If in a given meiosis, there is 0 crossover between two loci, then the two alleles from the same haplotype will end up in the same gamete. If there is 1 crossover, then the two alleles from the same haplotype end up in different gametes. If there are 2 crossovers between two loci, then the two alleles from the same haplotype will end up in the same gamete.
In short, if the number of crossovers between two loci (which expected value is the number of Morgans) is even, then the two alleles from the same haplotype will end up in the same gamete.
At very low Morgan (say 0.000001M), the probability of having an odd number of crossovers is low and the recombination rate is therefore low. As the number of Morgans increases, this probability of having an even number of crossover approaches 0.5. The recombination rate can therefore never be greater than 0.5.
Physical distance
Note that as the recombination rate per nucleotide varies throughout the genome (and among genders and among lineages), the distance in Morgan between two loci is not a simple function of their physical distance in number of nucleotides. The two are obviously correlated though.
Human genome
In the human genome, the average per nucleotide recombination rate is of the order $5\cdot 10^{-8}$ (Wang et al. 2012). This means that 1 cM is about 1.5 millions of nucleotides.
Highly Related posts
This question has actually been answered several times already. You'll find more information, some drawings and some math at the posts

Recombination frequencies
Genetic linkage greater than 50 centimorgans

For a more introductory post, have a look at

Why do we need two markers to measure a recombination rate?

The Morgan is a unit of how likely two traits will be conveyed together in offspring - also known as linkage.
Centimorgan's are not physical distances because the chromosome has specific variations in how well it crosses over when it recombines.
For instance in men and women there are more crossovers and this makes the genes appear to be further apart as they don't translate together in Meiosis...

The recombination frequency of two genes on the same chromosome is expressed in centimorgans (cM).
1% recombination frequency is a distance of 1 centimorgan (cM) on the gene map.
1 centimorgan roughly corresponds to one million base pairs of DNA.
The actual distance between two genes on a chromosome may vary, but this serves as a useful approximation to estimate the distance between two genes on a chromosome, in terms of the number of base pairs.

1% recombination frequency is a distance of 1 centimorgan (cM) on the gene map is wrong. It is a good approximation but is not correct. Please have a look at my answer for more info.

1 centimorgan is equivalent to the percent recombination frequency for 2 genes during the crossing over step of meiosis. You can calculate it with
(number of recombinant offspring)/(total number of offspring) * 100%
and the result will be in cM (centimorgans).
If you have many offspring that are recombinant for the 2 genes, you can see that you'll get a high percent recombination and therefore linkage (not physical) distance. Since there are many recombinant offspring, it can be inferred that the 2 genes have a lower likelihood of translocating together, since they are likely to be physically distant.
In the case where you have very few offspring that are recombinant, you'll get a low percent recombination and linkage distance because 2 genes that are close together have a greater likelihood of being translocated together during crossing over.

This is actually wrong. You are confusing a distance in cM with a probability of recombining. They are not quite the same (also they are good approximation for closely linked loci). Please have a look at my answer or to  the two posts I linked at the end of my answer.

Oops, my mistake. Isn't looking at recombinant offspring a "good" metric for inferring probability of recombining, though?

Yes it is but it is not the issue here. The distance in cM is not equal to the probability (in percent) of recombination. It is approximatively equal for low distance but start to get widely different for higher distances.


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Any good fish books out there?
I recently read "What a Fish Knows: The Inner Lives of Our Underwater Cousins" by Jonathan Balcombe. The first part was the best where the author explained how fish are very advanced creatures because they have been around a lot longer than other vetebrates.
Are there any other books out there similar to this one? There seem to be tons of bird research books. Of course, birds are relatively easier to study than fish. (Their size and ability to fly makes them difficult to track. But, at least they are not underwater and sometimes stay in one area for awhile. Fish are pretty much constantly on the move.)
I am not really looking for a text book unless you know of one that is interesting to read and not just a list of facts...unless a text book would be a good place to start.
I have read Colin Tudge's books on trees and birds. I wish he would write one on fish.

As a fisheries biologist these are what I would recommend to read.These are all science entertainment books(i.e., factual, but fun to read).The first 2 are more fish biology. The second  2 is more fisheries ecology.

Your Inner Fish: A Journey Into the 3.5-Billion-Year History of the human body.
Neil shubin
Demon Fish
Juliet Eilperin
Four Fish: The Future of the Last Wild Food
Paul Greenberg
Cod: A Biography Of The Fish That Changed The World
Mark kurlansky


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Do leaves grow larger by adding cells at the centre or at the edge?
I'm writing a paper on wrinkling of plant leaves. For biological and physical background information, I would like to know whether leaves grow by adding cells at the edge, at the center or in a completely different way. Since I need to confirm any information I get, please do not write opinions or guesses. It would be great if someone could find a reliable source with link since all my researches didn't lead to a good answer to this question.
Thanks in advance!

Welcome to Biology SE! Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Hello, I think you misunderstood my request. I'm currently writing my bachelor thesis in physics and thought that some biological context in the introduction would be nice. Since I do not understand most of the literature in biology, I would be glad if someone could explain in easy words how plant leaves grow. If my question is still inappropriate, feel free to close or delete.

Plant leaves develop from leaf primordium or meristem tissue (this tissue has special properties that allow it to continue dividing to make more more cells, i.e. stem cells - not stem cells like cells in the stem but the technical term 'stem cells). Because of the hormone balances to maintain this division property the meristem tissue will remain close to the stem or branch of the plant at the base of the leaf whilst the new cells added to the leaf slowly move outwards.
https://www.sciencedirect.com/science/article/pii/S1369526616300929


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Why not self pollination for finding the genotype instead of test cross?
Test cross can tell us what's the genotype of a plant is. But we can know that even by self pollinating the plant. For example,
If a garden pea plant has the genotype TT, then self pollinating them will give all tall plants.
If the plant has the genotype Tt, then self pollinating them will give both tall and dwarf plants in 3:1 ratio.
So we can simply say that by self pollination if all the plants are of same type then the parent plant is homozygous. If the plants are in ratio them the parent plant is heterozygous.

Because for test cross you need to phenotype far less progeny to be reasonably sure about parent genotype. Lets say you decide to phenotype N progeny. If the tested parent is heterozygote the random chance of you getting all N plants tall is (1/2)N for test cross and (3/4)N for self pollination.
So for example if you decide to phenotype N=8 progeny plants in case of self pollination (3/4)8=10% of your heterozygous parents will be wrongly assigned as homozygous which is error too high for almost anything serious. In case of test cross (1/2)8=0.4% of your heterozygous parents will be wrongly assigned as homozygous. To achieve the similar level of accuracy with self pollination you would have to phenotype N=19 or N=20 progeny plants.
The difference does not seem like much when testing one parrent but if you need to test many the costs will add up.


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What is the minimum sample size to get reliable results in haplotype and nucleotide estimations?
Different software have different methods for estimating diversity and each method will have assumptions about the quantity of
data required to produce a reliable result. I am estimating the haplotype and nucleotide diversity by DnaSP6 program of Sanger sequences. I would like what is the minimum sample size requires to get reliable results.
Thanks in advance.

Can you provide a little more information regarding what methods you are trying to use? Can you indicate the specific feature of DnaSP6 you are trying to use? This program implements many different analyses, each of which likely has different requirements. What are your input data? Are they just reads or have you done any postprocessing? How many loci? How many individuals, 10, 100, 1000?

I am trying to estimate haplotype and nucleotide diversity using gene flow . My input data are fasta files from sanger sequences, they code an unique protein. I have in some cases for some groups 2 or 3 individuals and I though that It could not be enought

"in some cases for some groups" what cases, what groups? are these population groups, groups that are the same protein, regions of the gene?

I have 13 groups defined of the total dataset, all of them of the same protein. 2 of these 13 groups have a sample size of 3 individuals each of them

I'm still a little unclear on what the analysis looks like, but I'm going to assume for the sake of this answer that it's a single locus sequenced across multiple populations, with some number of individuals per population, and that the concern is that some of these populations are represented by only a few individuals. I'm also going to assume that the individuals are diploid, so you in fact have a little more data than it appears.
All the same, this paper indicates that n<5 individuals in a population leads to quite noisy estimates of $\pi$ and $h$ (section "The effect of sample size on haplotype and nucleotide diversities"). This is of course specific to a certain ~500bp region that they collected sequences for. That doesn't mean that you can't compute these metrics, only that they may not be very reliable.
For reference, the early Neanderthal genome papers compute some measures based on only the two copies present in their diploid genomes- of course, they are assisted by a large amount of modern human data for making comparisons. If you have supporting data from other populations, you may still be able to say something about the populations with few individuals. But you will likely have to use measures other than $\pi$ and $h$ to do so.
Some other tools that you might use to "borrow" information from other individuals outside those groups are ordination analyses such as PCA, or clustering tools like STRUCTURE. One way of thinking about how this works is that you can "embed" your populations with few individuals in the population structure of your overall dataset. This allows you to still learn from those populations even if the number of individuals is small. The Neanderthal papers implement versions of this, but with much more elaborate statistical frameworks, for a whole genome rather than just a single gene.
I'm not sure if DnaSP can carry out these analyses, but there are a lot of tools that do similar things, one tutorial here. Of course looking at the DnaSP manual is probably a good idea to see what you can do with your current tool.
Depending on your goals it may also be interesting to compute F-statistics across your populations, this is done by most population genetics tool suites. I used GenePop many years ago to do this, it appears to still work, though I am sure there are better alternatives now.
An important note is that most of these measures are purely descriptive, not inferential. Low sample size makes descriptive statistics noisy, but doesn't invalidate them. Inferential statistics are a bit more dangerous.

Thanks you Maximilian, my sequences are haploid and the other assumtions are correct.  I checked one article that use a sample size with n<3 for π and h (Host abundance and identity determine the epidemiology and evolution of a generalist plant virus in a wild ecosystem). However I would like to know what other measures than π and h  you mean to do. Thanks in advance

see edit with more info.

Thanks a lot Maiximilian for your properly answer. I will take consideration of your suggestions. Thanks


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Validated Protein-Protein interaction database for cancer
I need to use validated PPI data in my research. Is there any database of such validated (like Mass Spectrometry) database for cancer?


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The use of cytotoxic T-cells
The video below mentions whether the dendritic should call in a 'anti-virus force' or an 'army of bacteria killers'. The video goes on to talk about how bacteria is killed, using B-cells, but there's no mention of cytotoxic T-cells. Is the cytotoxic T-cells only for viral infections or is it for both?
https://youtu.be/zQGOcOUBi6s?t=2m42s   <-video is time stamped.
I don't study biology and the internet is confusing sometimes.

I didn't watch the video, but the answer you're probably looking for is that cytotoxic T cells are for intracellular infections -- that is, CTL target pathogens that grow inside one's own cells.  All viruses grow inside cells. Some bacteria also grow inside cells (e.g. tuberculosis, Listeria); those bacteria can (often) be effectively attacked by CTL. Many bacteria do not replicate inside cells, and for those, CTL aren't effective, but B cells (via antibody) and T helper cells (by recruiting other cell types and modifying inflammation) can still be effective.

This is all true. I would also add that an important function of cytotoxic T cells is to kill abnormal cells - such as cancers.


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How does the lymphatic system filter blood?
One of the main functions of the lymphatic system is to filter blood. How exactly is it done?
Its quite hard to find an exact answer.

Can you provide a reference? I've never heard of it being described as a blood filter before as it doesn't carry blood.

@OliverHouston My biology teacher told me 'how does the lymphatic system filter blood?' is there any filtering that takes place in the lymphatic system?

OK, I'd forgotten about the spleen being part of the lymph system... See the answer below.

The spleen is an integral part of the lymphatic system, and it is a major filter of blood.
The way this is done is by removing old, distorted, or antibody-coated red blood cells from circulation.
Interestingly, the spleen is enlarged with many leukemias and lymphomas.

Need more detail, just enough to know I'm on track.


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Trying to extract DNA with an incomplete kit
I'm wanting to run a DNA extraction on soil and root samples using a 96-well plate kit.
My problem is that someone has gone through the kit and taken the Sealing Tape. This tape it used to seal the plates so they can be vortexed and centrifuged.
I have considered using a similar tape from our qPCR reactions, but this would be a very expensive last resort. I've tried filling a plate with water and covering it with strips of label tape, but the tape doesn't provide a good enough seal for the vortex.
I'm wondering if anyone has run into a similar situation, and if they were able to find a solution. This particular kit is this PowerSoil kit from MoBio, which no longer exists after being bought out by Qiagen. I called Qiagen and they do not sell the Sealing Tape individually.
Thank you

I use something like this for crystallography.

It is the vortex step that is causing you the trouble. But you can vortex manually, by pipetting up and down a few times in the well. Then seal the top of the plate with parafilm for centrifugation.