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What are the frequency ranges of most marine mammal vocalizations?
I am trying to determine a list of frequency ranges into which marine mammal vocalizations fall.
Ideally, I would like a list showing where the most popular marine mammal vocalizations fall, followed by the species name. That being said, I only really care about frequencies above 20 kHz, should they exist.
Example: (Numbers fabricated)

Orcas       : 30-40 kHz
Dolphins    : 100 kHz
Blue Whales : 60-88 kHz

etc.
Even if the list is 'quick and dirty', thats ok. The list will essentially point me to which species' songs/sounds I need to study.
Some additional context, this wikipedia link as well as this one have some nice sound files of many marine mammals' songs/sounds. I am trying to avoid having to download each one and analyze their spectral content. (I could, but would rather not).

Are you trying to find a list of frequency ranges, a range into which most vocalizations fall, or a list of marine mammals which vocalize above 20 kHz? It's three different (but similar) questions.

@Shep I edited.

Here there are spectrograms from Bottlenose dolphins (Tursiops truncatus), Killer whales (Orcinus orca) and False killer whales (Pseudorca crassidens).
Here there are spectrograms for Humpback whale (Megaptera novaeangliae) and from Sperm whales (Physeter catodon or Physeter marcocephalus)
Here there are spectrograms from Blue whale, Fin whale and Minke whale.
Some other google search for "spectrogram + your preferred cetaceans" should make your list. Enjoy.

Thank you. The majority seem to fall under ~20 KHz. Is this more or less true of marine mammals?

Dolphins can hear above 110 kHz, and produce vocalizations in this range.  Clicking has evolved in proposes and sperm whales and is predominantly above 100 kHz (to avoid being heard by killer whales). It's a bit subjective, of course: if you do a frequency decomposition of a click, it will always have some component with very high frequency.
That dolphins have evolved into such an niche highlights a problem with asking about "most" marine mammals, though: evolution often favors diversification between species, so you'd expect very different vocal ranges, to the point that many species have no overlap at all. (for the sake of illustration, ask yourself where most people live)

Thank you Shep I have edited the post for additional info/context.

Dwarf and Pygmy sperm whale clicks contain energy above 100 kHz, but sperm whales actually have lower frequency clicks with most energy below 20 kHz.

Baleen whale calls are typically low frequency (less than 5 kHz), with blue whales and fin whales producing the lowest frequency calls ranging from about 10 - 100 Hz, and some minke whale and humpback whale calls can extend up to 24 kHz.
Sperm whale echolocation clicks range from 500 Hz to 30 kHz.  Dolphin whistles typically range from 1 to 25 kHz, though some orca whistles are above 30 kHz.  Most dolphin echolocation clicks range from 5 to 130 kHz, while some dolphins, porpoise, and kogia species (dwarf and pygmy sperm whales) produce narrow-band high-frequency clicks in the 100 to 130 kHz range.
https://cetsound.noaa.gov/Assets/cetsound/documents/Roadmap/ONS_Roadmap_Final_AppendixA.pdf

Hi and welcome to Bio.SE. Thanks for posting. However, please provide support for your claims. Unsupported posts come across as opinions and are best reserved for comments. We have high expectations of good answers on this site to help avoid the spread of misinformation. Please consider revising your answer to provide some sort of support to attract more positive attention and to better (and more accurately) inform our future visitors. Thanks!

All toothed whale echolocation clicks fall above 20 kHz (except sperm whales).
In addition to echolocation, porpoises and some of the small dolphin species also use ~130 kHz clicks for communication.
If you are interested in echolocation click frequencies, then this paper (which I co-authored) provides a detailed comparison and discussion of the frequency content of toothed whale clicks.
This paper also includes a table (Document S1. Table S1.) that summarizes biosonar click parameters of some 38 toothed whale species.
When acoustic recorders are placed directly on species like porpoises, frequencies above 200 kHz can be recorded, but it is only the energy below ~150 kHz that is likely to be relevant for echolocation, as this is about the upper hearing limit of porpoises and other small cetaceans (you can find an overview of audiograms and references on marine mammal hearing in this paper).
References
Sørensen, P. M., Wisniewska, D. M., Jensen, F. H., Johnson, M., Teilmann, J., & Madsen, P. T. (2018). Click communication in wild harbour porpoises (Phocoena phocoena). Scientific Reports, 8(1), 1-11.
Jensen, F. H., Johnson, M., Ladegaard, M., Wisniewska, D. M., & Madsen, P. T. (2018). Narrow acoustic field of view drives frequency scaling in toothed whale biosonar. Current Biology, 28(23), 3878-3885.
Southall, B. L., Finneran, J. J., Reichmuth, C., Nachtigall, P. E., Ketten, D. R., Bowles, A. E., ... & Tyack, P. L. (2019). Marine mammal noise exposure criteria: updated scientific recommendations for residual hearing effects. Aquatic Mammals, 45(2).

A quick reference point is dosits.org; their audio gallery has additional information on the species and references. This reference site was developed based on research (and much of it by researchers), so it is reasonably trustworthy and I suspect they update it periodically.
In general, above 20kHz is the realm of dolphins/porpoises. Echolocation clicks are short broadband clicks-- so they cover a very wide range of frequencies in a short little clicks.


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MRI maximum field strength
More tesla = more resolution, is there limit of human body of how much strong magnetic fields it can handle safely which means there is limit to how strong MRI magnets we can use?
Engineering problems aside, could we scan live humans if we had 20 or 40 tesla MRI machine?

What have you found while trying to answer the question?

Technically, higher main magnetic field strength doesn't mean more resolution.  There are three parts to the scanner: 1) main magnetic field, 2) gradient coils and 3) RF coils.
The main magnetic field strength (1.5T, 3T, 7T, 9T, the last two typically more for research) determine more of the signal to noise (in a very simple sense).  This is static - it doesn't ever change.
The gradient coils are what determines the resolution and the rate of switching is the biggest determining factor. There are limits on what they can switch at when used on humans as they can cause peripheral nerve stimulation, vertigo, nausea, metallic tastes etc.
I don't believe static field of 20T etc would be a problem, though there is not much research to prove or disprove that.  The problem would be moving into that field as that will cause the same types of effects as the gradient coils switching.  Even for 7T, one must not run into the scan room as it can cause peripheral nerve stimulation (and some other effects). Currently, I believe the strongest full body human MRI scanner is 10.5T. Another article talks about 11.7T human scanners (one of them is a "head only" scanner. It also has some nice pictures).

Thanks for the nice answer, I think you meant 11.7T.

is there limit of human body of how much strong magnetic fields it can handle safely which means there is limit to how strong MRI magnets we can use?

The 2018 {1} study concluded:

Where feasible, effects are quantified for magnetic fields beyond 7T with the conclusion that there are no foreseen barriers either in the technical or human safety aspects of brain MRI and MRS at fields up to 20T. This conclusion is conditioned on results of recommended experiments to verify the predicted level of physiological effects beyond 9.4T. This technology is predicted to enable quantification of biochemical components of the functioning brain not detectable heretofore.

FYI:

MRI scanners in the United States with teslas
The strongest MRI for small animals — 21.1 teslas — is located at the National MagLab's headquarters in Tallahassee, Florida. (mirror)
https://www.openwater.cc: "Rivaling MRI quality at a fraction of the price and size".

References:

{1} Budinger, Thomas F., and Mark D. Bird. "MRI and MRS of the human brain at magnetic fields of 14 T to 20 T: Technical feasibility, safety, and neuroscience horizons." NeuroImage 168 (2018): 509-531. https://www.ncbi.nlm.nih.gov/pubmed/28179167

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Why is the central tendon of diaphragm called a tendon?
Why is the central tendon of diaphragm called a tendon when it does not connect the diaphragm to any bone?

Is there a requirement that tendons attach to bones? Histologically, it's just dense connective tissue.

@kmm Ligaments are similar to tendons and fasciae as they are all made of connective tissue. The differences in them are in the connections that they make: ligaments connect one bone to another bone, tendons connect muscle to bone, and fasciae connect muscles to other muscles.        Wont this result in no difference in three,  if tendon wont connect muscle to bone or something(like lens of eye)?

Not all ligaments connect one bone to another bone. ex; ligaments of liver which connect liver to abdomen, and other organs.

The basic difference between ligament and tendon is that one restricts movements while other aides in movement.

A tendon usually connects a muscle to a bone, but not always.
According to InnerBody, the diaphragm muscle originates at the lumbar vertebra, lower ribs and sternum and inserts to the central tendon.

The central tendon — a flat aponeurosis made of dense collagen fibers
  — acts as the tough insertion point of the muscles.

So, the central tendon acts as the diaphragm's own insertion.
A similar example is aponeurosis of the external oblique muscle in the lower part of the abdominal wall (Brazosport.edu, Picture 10.11.a.).
A tendon is the connective tissue that is always a part of a muscle and it fixes the muscle during its contraction.
A ligament is the connective tissue that merely connects two bones or two internal organs and is not actively involved in their movements.

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How is cartilage immunised?
How is human cartilage immunised (protected) against pathogens since it does not contain lymphatic vessels?

I also had this relevant problem, when I was learning about cartilage tissue.
Generally, cartilage tissue has no blood supply. But it is a traversable  tissue, therefore nutrients, and breathing gases can enter into the tissue without any problem.
But the problem is how does it immunized while there is not containing of lymphatic cells.
The perichondrium, has a presence  of blood vessels. It pulls/stimulate  the necessaries for enter to the cartlage tissue. That's how, the  tissue get immunized.

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How does cartilage become bone?
It's a famous fact that bones begin as cartilage and later become bone, but I never was clear how exactly
 this changeover occurs. Could someone please explain this to me?

What research have you done? What exactly you are unable to understand? Show your efforts.

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

FYI: Why is cartilage replaced by bones in an vertebrae adult?

The process is called endochondral ossification.
It is important to point out that not all bone is derived from cartilage. For example, when a bone is fractured and is healing, the new bone does not always come from cartilage, rather intramembranous ossification occurs. There are therefore multiple mechanisms at a microscopic level by which bone may form. Additionally, bone formation in the long bones is different to that in, for example, the flat bones of the skull.


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How is yellow elastic cartilage a true cartilage?
My book has only mentioned the fact but no reason is given so I would like to know the reason for it. I would like to know what more to add in the body but the question just doesn't get posted.

What research have you done , have tried googling it atleast? Question which doesn't show attempt are likely to be deleted.

Yes i have already googled it even asked the same question but it always open wikipedia which donot provide me my answers

Could you cite the book?

A TEXT BOOK OF BIOLOGY

author name pls

Wikipedia cartilage defines it as being composed of specialized cells called chondrocytes that produce a large amount of collagenous extracellular matrix, abundant ground substance that is rich in proteoglycan and elastin fibers. , then states that: Cartilage is classified in three types, elastic cartilage, hyaline cartilage and fibrocartilage, which differ in relative amounts of collagen and proteoglycan. The term elastic cartilage links to a separate page describing elastic or yellow cartilage. What other information do you need?

Maybe he wants the reason why its called "true"

https://books.google.co.in/books?id=uIWU4x4Rq0cC&pg=PA32&lpg=PA32&dq=%22true+cartilage%22&source=bl&ots=GNYGWHvaR4&sig=O__pwHVGQjZEerZvASTSTbUDwOk&hl=en&sa=X&ved=0ahUKEwjT87G7tJ7VAhUmTY8KHQOICyMQ6AEIQDAI#v=onepage&q=%22true%20cartilage%22&f=false

jm97 it the book i mentioned is by...Dr.Rameshwar p.singh,Dr.Shree krishna subedi,Mukti ram aryal and Dinesh chandra adhikari....and i what i want to know is mentioned in title

True cartilage is something of a simplification or a misnomer, they are saying that it truly a form of cartilage and not another elastic tissue type. in fact
"true cartilage" is a term coined by your book. They could have also said it's part of the cartilage family of cell/tissue types.
It's similar to cartilage under a microscope, structurally and has similar consituents, although yellow cartilage also contains elastin. If you were to dissect humans, you would probably find that there are a lot of variations of cartilage of different elasticity, midway in between both forms.
this page is full of info and pics:
It's a good idea to check wikipedia and 2-3 pages to find results to that kind of query, you will find fabulous resources, whereas on stack it is really for studies that take more than 20 minutes via google.


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What is the meaning of Dimer Catastrophe?
What is the meaning of Dimer Catastrophe?  I still don't understand it even I've already read the paper about it.  Here's the link to the paper origin NCBI

A "plasmid dimer" is defined as a plasmid that has two origins of replication instead of the usual one origin of replication. This can happen if two copies of the same dimer undergo recombination resulting in one plasmid with two origins and one with zero. I hadn't seen this term before, but it seems to be the meaning with which it's used in this paper and a few others I saw.
The "dimer catastrophe" hypothesized in this paper refers to the idea that over time this would lead to a reduction in overall plasmid copy number (and thus an increased probability of plasmid loss), since dimers may be more likely to replicate than monomers (due to having more origins of replication).
For what it's worth, I also found the paper you linked a bit hard to understand, but I found this one more explanatory (your mileage may vary): Multicopy plasmid stability: Revisiting the dimer catastrophe.


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Is there any stem cell or biogel method that exist for muscle and tendon lengthening?
Is there any stem cell or biogel method that exist for muscle and tendon lengthening?
It is known that height surgery is limit to six inches with two surgeries and three inches each, it is also true that there is limit because the muscle and tendons could stretch no more. Is there some research about this?

In doing search into muscle stem cells, I found some articles which discuss roles of satellite stem cells and non satellite cells  involved in muscle regeneration: (Yin, Price and Rudnicki, 2013,Seale and Rudnicki, 2000, and Mitchell et al, 2010).
Other articles, that I found discussed the splicing of insulin-like growth factors (IGF-1) into the satellite stem cells rodent muscles and the subsequent expression of the gene were studied to understand how is plays a role in muscle repair (Hill and Goldspink, 2003, Musaro et al, 2004). Another study looked at how transforming growth factor-β (TGF-β) and its interaction in the Notch signaling pathway play a role in smooth muscle repair (Kurpiinski et al, 2010)( Review Articles by Péault et al, 2007  and Seagers and Lee, 2008 )
As for current methods on the application of stem cells to myogeneration or myoregeneration, there are a few papers that I found but, it seems like we are still too far away from anything that is medically feasible (Zhu et al, 2014, Milner and Cameron, 2013)
Hopefully that answered your question or at least put you on the right track in your research.
EDIT: I found some papers on tendon repair and growth, but the conclusions are the same, in that there is much more research and technology improvements to be done (Awad et al, 2007 and Breidenbach et al, 2014)

Limb lengthening surgery is usually used to treat sequelae caused by bone disease, trauma, pygmyism or inflammation. I personally do not recommend to use surgical methods to increase height. Typically Limb Lengthening requires Achilles pre-lengthening surgery and a lot of postoperative rehabilitation. Moreover, Limb lengthening surgery may cause pain, infection, muscle atrophy, joint stiffness and delayed bone healing. There's a lot of related research cause this study is timely for some patients.
ALDEGHERI, R., RENZI-BRIVIO, L., & AGOSTINI, S. (1989). The callotasis method of limb lengthening. Clinical Orthopaedics and Related Research, 241, 137-145.
De Bastiani, G., Aldegheri, R., Renzi-Brivio, L., & Trivella, G. (1987). Limb lengthening by callus distraction (callotasis). Journal of Pediatric Orthopaedics, 7(2), 129-134.
Paley, D. (1988). Current techniques of limb lengthening. Journal of Pediatric Orthopaedics, 8(1), 73-92.
Paley, D. (1990). Problems, obstacles, and complications of limb lengthening by the ilizarov technique. Clinical Orthopaedics and Related Research, 250, 81-104.
Szoke, G., Lee, S. H., Simpson, A. H., & Prescott, J. (2005). Response of the tendon during limb lengthening. The Journal of Bone and Joint Surgery.British Volume, 87(4), 583-587.

It seems that just a Russian researcher named Dr Alexander Teplyashin has made any progress into using stem cells for LL (Limb lengthening). Conventional way to go about it would always be surgeries which are detailed in Wikipedia (reference). This is a relatively new development, so I could not find any relative publications to support the claim of this particular researcher. There is however a website detailing the news in English, most others being in Russian (reference) Here are a few publications of his (reference). There are already lengthening methods available which is a combination of both surgery and stem cells (reference). As far as there is some credible proof, I would take the claims of that Russian researcher with a pinch of salt.

I upvoted it, however it is bone lengthening, not the muscle and tendon lengthening i asked


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Lifespan of connective tissue cells
This post is regarding a follow up on my initial post on "Properties and life cycle of chondrocytes and tenocytes".
I am elaborating on my question on the lifespan of tenocytes and chondrocytes.
From what I have read, tenocytes and chondrocytes form from mature stem cells, more specifically Mesenchymal stem cells. These cells can replicate through mitosis, and are present in the body in different tissues like bone marrow. These cells are the key in the regeneration of diverse tissues.
When the cells that inhabit tendons or cartilage die, do new MS cells travel to the tendon or cartilage area and diffentiate into a new tenocyte or chondrocyte? Are tenocytes and chondrocytes continuously replaced?

"This post is regarding a follow up on my initial post on "Properties and life cycle of chondrocytes and tenocytes". -> could you please add a link to this post? I couldn't find it. Thanks!

Not that I'm aware of. There isn't any blood flow to either tendons or cartilage as an adult, so the pathway for migration doesn't exist.
Tendons and cartilage are tissues composed of dead cells after their formation (the cartilage growth plates cease to exist in your teen and completely ossify, tendons I'm not sure on). Damage to tendons and cartilage is permanent, and can cause arthritis (when the cartilage is completely worn away and bone-on-bone contact occurs at joints).
Unlike living tissue, because tendon cells are dead, they are much, much easier to transplant - they do not produce any signaling molecules or have any surface proteins which would trigger an immune reaction for the vast majority of people. Shoulder surgeries often utilize this to the benefit of the patient, especially acromio-clavicular injuries.
If living cells are brought to the dead tissue, some repair is initiated, as I do recall a technique where surgeons tapped into the marrow of a patient's femur to stimulate cartilage reconstruction, but I also remember reading that the new cartilage formed wasn't the same hyaline cartilage produced by chondrocytes of the growth plate, so the repairs were temporary.
Artificially produced tendons do exist, and many are braided in order to foster interaction with host tissues (when you suffer from tendonitis, the tendon itself isn't repaired - the tissue around the tendon is repaired and strengthened). I'm not aware of any successful attempts to regrow tendons.
Attempts to grow cartilage in vitro have been successful, but re-introducing it into the body to produce a surface to articulate against has presented significant difficulties. Because we cannot (currently) reproduce biological articular surfaces, joint replacement often uses composites or surgical grade metals (both of which present problems of their own, but arthritis is not one as there's no living tissue to feel pain).

I am a bit puzzled by two of your statements, could you comment on them? 1) "There isn't any blood flow to either tendons or cartilage as an adult, so the pathway for migration doesn't exist.". Since when migration needs blood flow? Plenty of cells (neurons, for instance) migrate using the extracellular matrix as a guide. 2) "Unlike living tissue, because tendon cells are dead [...] they do not produce any signaling molecules or have any surface proteins which would trigger an immune reaction": so... you mean collagen and proteoglycanes are not allergenic?

Also, adding some references will improve the quality of the answer.

@nico
The normal route for cellular migration is the circulatory system.
Collagen almost never produces an allergic reaction. Proteoglycans vary.
As an update: I was apparently out of date with tendons. Tenocytes do perform repairs, but it might take a while (as-in, measured over months or years for significant damage). -Riley, G. (2004). "The pathogenesis of tendinopathy. A molecular perspective"
Cartilage would be repaired by chondrocytes, which inhabit the lacunae of bones. Cartilage lacks lacunae. Chondrocytes, literally, cannot reach damaged cartilage unless the damage reaches bone.

I beg to differ on the circulatory system being the normal route for cellular migration. It is one of the routes for migration, surely, if you think of the immune system but, again, there are counterexamples, neuronal migration being probably the most obvious.

Then you're free to differ. To the limit of my knowledge the normal route for cell migration throughout the body is either the circulatory or lympathic systems, as those systems span the entire body. If the majority of cells use a separate route, then I am not aware of it. Neurons - as much "migration" as occurs with them after adulthood - are special cells to begin with. I'm not saying you're wrong, but I'm unaware of other major routes.

Just to clarify, what I disagree on is the term normal. For neurons you may want to have a look at the rostral migratory stream

Then define the most common route of cellular migration in the human body as you see it.
I'm not saying you're wrong, but just repeating "Neurons do it differently" isn't the same as proving I'm wrong.

I just think there are different routes, I do not like the use of the term normal because it implies the others are "anormal". Semantics, probably. Anyway, I would say that, for instance, during development many cells do not migrate through bloodstream, but rather in the extracellular matrix of the tissue.

Anyway, my point is: you cannot say that tenocytes cannot migrate in the tendons BECAUSE there is no blood vessels. This is obviously false, as there are counterexamples of cells that migrate without needing blood vessels. New cells may as well be born from locally present stem cells, as it is the case in other tissues.

Allow me a moment to be just as pedantic as you. If you're talking specifically about tenocytes, and you are right above, then the vascular system is the ONLY common path for migration out of the bone marrow from their mesenchymal stem cell progenitors. There aren't any stem cells in the somatic muscle tissue. They just don't exist, otherwise tendons might heal much, much faster.
For the rest of your tangent about cellular migratory paths, I don't see how they relate to the original question - much less how they're anything other than your opinion when you can't back up your answers.

Come on, do not take it personally. What you are saying is exactly why I am asking for references. Your answer just says: "there is no blood stream hence cell cannot migrate". Sorry, but I consider that a bad explanation. Progenitors could get near the tendon via bloodstream and then migrate through the collagen fiber. Immune cells do that, for instance during tendinitis. I am not being pedantic, but -because I am far from being an expert in tendons- I do need references to decide how to vote on your answer. If you are willing to answer the question the burden of proof is on you, not on me.

You have the burden of proof. You do not contest my initial assessment of whether or not tendons/cartilage are capable of repair, but my use of the word 'normal'. That's a separate debate which you started. You continued by naming a single cell type (Neurons) which use an alternate method, and failed to provide any other examples while it's common knowledge that the vascular system ferries Erythrocytes, Leukocytes, and Platelets all the time. Then your example of progenitor migration (which doesn't happen anyways) still uses the vascular system to migrate to the tendon.

If that's not the definition of pedantic, I don't know what is, and I'm not debating the topic with someone I don't believe has a firm grasp on basic human anatomy and physiology.

wow, we are down to personal offense now. How poor. By the way, I have a PhD in physiology so, yes, I have a basic grasp on it. Anyway, I will be happy to remove my downvote when you will add some proper references. Have a good day.

let us continue this discussion in chat


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Normal Frequencies in Heart
I am trying to visualise possible ranges of frequencies from different structures of heart:

different valves and their possible frequencies
heart sounds I - IV and their normal frequencties
what can frequencies be in healthy situation for adult
what can frequencies be in healthy situation for children 4-9 years old

I searched meta-analysis, clinical trials and reviews in PubMed unsuccessfully.
Is there any review article or book about the frequencies from different structures of heart?
Search terms used

frequency heart
frequency heart valve

frequency as in the electromagnetic frequencies I presume?

Yes. Electromagnetic frequencies.


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What are the trajectories of flying insects?
Many flying insects tend to have very jagged trajectories. For moves of a fruit fly looks like a random walk.
Is there any research on the properties of trajectories (e.g. their fractal dimension or mathematical models producing similar behaviour)?
Besides the path of a single insect, I am also interested in the interaction of a small number of insects (e.g. 2 or 3).
I am aware of the research in flocking and swarming (e.g. Tamas Vicsek, Anna Zafiris, Collective motion 2010) and of techniques of obtaining such trajectories (e.g. Danping Zou, Yan Qiu Chen, Acquiring 3D motion trajectories of large numbers of swarming animals or an open access pdf, 2009). However, I haven't found within them an answer to my particular question.

I'm curious what is your purpose in consideration of insect movements in isolation of their function (avoiding predators, looking for prey, finding new habitat patch etc.)

@MartaCz-C: Abstraction sometimes helps (I am a physicists). And properties of the trajectory are very likely in a close relationship both to optimizing certain actions  (avoiding predators, looking for prey, finding new habitat patch etc.) while being bounded by constrains (physiological, energy, ...).

Quick search - Some articles that may interest you:

Random walk model of insect movements

Kareiva P. M., Shigesada N. (1983). Analyzing insect movement as a correlated random walk. Oecologia 56(2-3) 234-238

Artificial life model of flying insects and its comparison to real insects navigation strategies.

Dale K., Collett T. C. (2001). Using artificial evolution and selection to model insect navigation. Current Biology 11(17) 1305–1316

The last one is not about insects, but it's a trial to practical usage of the mathematical analisys of invertebrate movements.

Shimizu N. et al. (2002). Fractal analysis of Daphnia motion for acute toxicity bioassay. Environmental Toxicology 17(5) 441–448

This is not an answer but a list of references. Whether accepted by the poster or upvoted by the hoi polloi, it should be edited to provide an explanation (unlikely after ten years) or converted to series of comments and then deleted by the mods.

Dickinson (2005) has a good review of insect flight, including behavior, biomechanics, electrophysiology, and neural control with links to more of the primary literature. What follows is a general summary thereof.
The jagged trajectories you mention are called saccades in the insect flight literature. In Drosophila, saccades are ~90° turns accomplished in approximately 50 ms. Because flies can't move their eyes independently of their heads, saccades are though to allow a relatively constant visual field most of the time, interspersed with rapid reorientations during which the fly is "blind."
The actual turn begins with the generation of a torque, which starts the fly turning. Shortly thereafter, the halteres sense this change and a counter-torque is produces, which stops the turn.
Rather than random turns, Drosophila are turning away from visual expansion as they near objects. So as they move closer to an object, it expands in their visual field, and they turn away from it.

Thanks, a good and informative answer. However, I am interested not only in saccades but the whole patterns of movement (so also structures at different time scales, e.g. minutes).


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Compare and contrast "Rubisco activity" and "assimilation rate" (is there a difference, and if so, what is it)?
I am confused about the variable "RuBisCO activity". How is it measured, and is it any different from the net assimilation rate?
Based on some background reading (e.g. Kling, 2008; Lambers et al 2011)  the only difference that I can find is the units. Both would have "carbon fixed per unit time", but RuBisCO activity is expressed per unit mass of the enzyme, while assimilation rate is per unit leaf area (or less commonly, leaf mass).

Both are measures of carbon fixation rate.
RuBisCO activity specifically refers to the rate at which the enzyme RuBisCO fixes carbon to RuBP, and is measured by isolating the enzyme from tissue samples and, usually, using radiolabelled CO2 to measure how much carbon is fixed in a set amount of time in controlled conditions and with controlled supply of substrate.
Carbon assimilation rate is generally a whole-plant or whole-leaf variable, measured on a larger scale. It is usually measured by measuring leaf sugar carbon before and after a set period, again using radiolabelling. Conditions may or may not be controlled, and it can be measured in the field (unlike RuBisCO activity).
RuBisCO activity might differ from net fixation in the short term in plants which have an intermediate carbon fixation step, such as in CAM or C4 plants, if the net fixation measurement includes the intermediates - the pool of intermediate carbon-containing molecules have technically been fixed but not by RuBisCO. However, over longer time periods this effect will disappear, as ultimately all CO2 is fixed or re-fixed through RuBisCO.

This is a useful answer, and it does answer my question. However, I was not familiar with measuring assimilation using 14C-CO2. Almost every leaf-level measurement I have found in the literature has been measured with a LI-6400, which measures exchange of [CO2] and [H2O] between the leaf and atmosphere. In what cases is 14C used?

Are you asking for specific cases, or a general reason why people would choose 14C?

more or less in general. It seems like a less direct measure (since the sugar pool presumably has losses to respiration as well as inputs from assimilation). It also seems more difficult in general, although perhaps less expensive.


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On the effect of polluted air on health. Is it more gradual, or more immediate?
I've heard time and again that living in São Paulo (a large city in Brasil) takes 1.5 years from your life expectancy. The allegation is that this happens because of air pollution.
I am just wondering how air pollution harms humans. Is the effect cumulative? Or is it a more immediate effect that makes the elderly die sooner?

also: is there a better place for this question on the stack exchange network ?

I think it's fine for here, I removed the part about wanting to live there, as I think that doesn't have any bearing on the answer.

that's an interesting question, I've read once that the biggest concentration of centenarian was in Hong-kong, but they may have also more wealth and resources than people leaving in forests. But like you I wish I could live far away from that pollution cars/smokers/...

The main factors of urban air pollution are nitric oxides, carbon monoxide, and what is called in german "Feinstaub" (very small carbon-rich particles from diesel exhaust). However, do not forget heavy metals: street dust is especially metal-rich and is swept into the soil near the streets where children and farmed plants can take it up. Lead is a heavy metal that can be breathed in with the air. Last not least noise over a certain threshold is proven to be a cause of illness, even loss of life time (10 years near an airport, if I recall correctly, but airport noise is getting better while machines become more fuel-efficient).
To answer your question one would have to look at every single factor. Lead accumulates in bones and destroys your brain. I just see Brazil banned it too in the 80's so this one killer is no more.
http://en.wikipedia.org/wiki/Tetraethyllead
I have found a meta-study that reviews about 80 papers on the subject, especially the Sao Paulo studies, so this should fit exactly your questions:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093800/

Those 3 are the main problems, then ?
Which of those would fit the "cumulative effect" idea, and which would fit the "harms the elderly" ?

Please see the link I have added


text:
How would I explain different properties of the same protein in different species?
I recently finished an experiment where I analyzed the rate of ATP hydrolysis of Heat shock protein 104 in three species of fungi. They have shown to all have different rates of ATPase activity. How would I explain these findings based on structure/ATP affinity?  The experiment was done in vitro.
The species under consideration:
Candida albicans,
Saccharomyces cerevisiae,
Schizosaccharomyces pombe

The experiment was done in vitro?

Yep, it was done in vitro.

(i) I used an NADH-PK Linked Assay where I looked at the absorbance decrease when NADH is oxidized to NAD+. They were all pure proteins. (see: NADH-coupled microplate photometric assay for kinetic studies of ATP-hydrolyzing enzymes with low and high specific activities) (ii) All the Km values were different, ranging from 2mM-4mM and I used ATP concentrations ranging from 0mM to 10mM.

Have you checked sequence similarity/identity, especially of the nucleotide contacting regions (otherwise known as the P-loops I think)?

Do you know any databases where I could find the amino acid sequences of these protein orthologs?

The NCBI protein database or UniProtKB would be the first places I would search. Other databases exist, but these are my personal favourites

What TomD says about contributing proteins, here's an excerpt from the InterPro entry: A small adaptor-like protein, ClpS, modulates the activity of ClpA and is an important regulatory factor for this protein [4]. It protects ClpA from autodegradation and appears to redirect its activity away from soluble proteins and toward aggregated proteins.

As nobody has answered this good question, I'll have a go.
Firstly, let me state that I have little-or-no knowledge of heat-shock
proteins. What follows are some general observations and thoughts.

It would not be unusual for the same enzyme from different
species to have different kinetic properties. For example, yeast and
horse liver alcohol dehydrogenase (EC 1.1.1.1) vary quite dramatically in this regard
(see below).
It is  to be expected that the same
protein from different species will have different amino acid sequences.
Even the sequence of cytochrome C (~104 amino acids), one of the most
conserved proteins, differs between species. There are 44 amino-acid differences
between human and yeast cyctochrome C, for example (although there is no
difference in amino acid sequence between the human and chimpanzee
proteins) [see Creighton, 1993, p116, quoted below].
This fact alone could explain the kinetic variation, but it might be
very difficult (and require a lot of work) to pinpoint what differences
in amino acid sequence (if any) account for the observed differences in
kinetic constants.
In the case of hsp104, a quick alignment (out of curiosity)
of the amino acid sequence of the  Saccharomyces
cerevisiae and Candida albicans enzymes showed quite a number of amino acid differences between these obviously homologous proteins.
I used the
TCoffee
sequence alignment algorithm (a new version of ClustalW) at the
xPASy server. (I received an alignment score of 98).
For the record, the accession numbers used are the following:
hsp140 from  Saccharomyces cerevisiae, 908 amino
acids, Accession Number AAA50477
hsp140 from Candida albicans, 899 amino acids, Accession
Number AAK60625
Of course, the observed kinetic differences may not be due to
amino acid sequence differences at all, or may not be
only due to such differences.  Post-translational
modification (such as phosphorylation) and differences in quaternary
structure are other possibilities.
I notice from this
reference (Parsell
et al., 1994)  that hsp104 from
Saccharomyces cerevisiae forms oligomers in the
presence of ATP, and this might be very important in any explanation of
kinetic differences. (My whole knowledge of hsp140 does not extend
beyond this excellent paper).
Yeast and horse liver alcohol dehydrogenase (ADH) are
homologues and catalyze an identical reaction.  Both also contain zinc.
However, the yeast enzyme is a
tetramer, whereas horse liver ADH is dimeric.
Another difference worth
pointing out is that in vivo yeast ADH functions as
an aldehyde reductase (making ethanol), whereas liver ADH functions as
an ethanol dehydrogenase (in alcohol elimination). [I am aware there are
other isozymes of yeast ADH, which may have different functions].
As an ethanol dehydrogenase, the yeast enzyme has a
kcat value of 455
s-1 (pH 7.05, 25oC;
Dickinson & Monger, 1973) whereas the horse liver enzyme has a
kcat value (for ethanol
dehydrogenation) of only 1.67 s-1 (pH 6.0,
25oC; Dalziel, 1962, 1963).
In the reverse direction, the
kcat for acetaldehyde reduction is
3850
s-1 for the yeast enzyme (pH 7.05,
25oC, Dickinson & Monger, 1973), whereas it
is only 125 s-1 for the liver oxidoreductase (pH
6.0, 25oC; Dalziel, 1962, 1963).
How can we explain these kinetic differences from an analysis of
structure? In my view this is a very tough question.  It may be due to some or all or none of the differences I have highlighted.
Perhaps the question needs to be rephrased as follows: Is there any fundamental
difference, at any level, in the catalytic mechanism, or in the form of the enzyme in
solution, or in the amino acid sequence, or in the tertiary or quaternary structure, that can reasonably account for the observed kinetic variation?
Are the differences worth explaining?  Perhaps one needs to go no further than to record the individual variation under rigorously-defined reproducible conditions?

Before such questions may be answered, it is important to establish the nature of the observed kinetic differences.  What follows are merely some guidelines, most of which you are probably aware of.

Is the velocity versus enzyme plot linear in all cases at both high and low substrate concentrations? That is, in kinetic jargon, is the   ν vs [Eo] linear?  As the enzyme is known to form oligomers in the presence of nucleotides (see above), this might be an important control.  Does doubling the enzyme concentration exactly double the rate, and does halving the enzyme concentration exactly half the rate (at both high and low substrate concentrations)?
An example of an enzyme where the ν vs [Eo] is often not linear is phosphofructokinase.
I notice you are using a coupled assay with two coupling enzymes.  What effect does doubling the amount of one and/or both of these enzymes have on the observed rate?  It should have none, otherwise the assay is not valid.
The substate is ATP.  Almost certainly, the 'true' substrate for the enzyme is MgATP2- (correct me if I am wrong about heat-shock proteins). How much Mg++ do you have there?
In determining kinetic parameters for ATP-utilizing enzymes one needs to be aware of ionic equilibria during experimental design. Failure to do so may give rise to spurious kinetic effects.
A solution containing ATP and Mg++ will contain many ions, probably only one of which is the substrate for the enzyme, and whose proportion will vary with concentration.  It is essential that this is taken into account. The problem and posssible solutions are explained very well by Cornish-Bowden (2003, pp 86 - 89) and by Storer & Cornish-Bowden (1976).
One experimental design is to keep the concentration of MgCl2 in constant excess over total ATP concentration (CB recommends 5mM).  This is an important one.
Are Michaelis-Menten kinetics obeyed in
all cases? Is there any evidence for substrate inhibition, or substrate
activation?
Are the double-reciprocal plots (Hanes plot,
Lineweaver-Burk plot, Eadie-Hofstee plot) linear in all cases?.  Non-linearity may be an indicator of kinetic complexity, or of poor experimental design.
If you plot the kinetic data for all three enzymes on a single double-reciprocal plot what sort of a pattern do you get?  Competitive? (no
differences in kcat, but
differences in Michaelis constants).
In comparing enzyme kinetic parameters the Michaelis constant has the big advantage that it is independent of enzyme concentration.  Thus any differences are likely to be 'real' and not due to errors in, say, protein concentration.
But what about Vmax? If, say, you determine that the maximum velocites differ by a factor of 1.4, can you be certain that you are not inadvertently adding slighly more enzyme in the higher case, and that the catalytic constants are in fact identical?
As I said above, these are just personal thoughts.  Most you probably already aware of.

References

Creighton, T.E. (1993) Proteins. Strutures and Molecular Properties. 2nd Edn. W.H. Freeman & Company.
Cornish-Bowden (2004) Fundamentals of Enzyme Kinetics 3rd Edn. Portland Press, London.
Dalziel, K. (1962) Kinetic Studies of Liver Alcohol Dehydrogenase. Biochemical Journal, 84, 244-254.[pdf]
Dalziel, K (1963) Kinetic Studies of Liver Alcohol Dehydrogenase and pH
with Coenzyme Preparations of High Purity.  J. Biol. Chem., 238,2850-2858. [pdf]
Dickinson, F.M. & Monger, G.P. (1973)  A study of the kinetics and mechanism of yeast alcohol dehydrogenase with a variety of substrates. Biochemical Journal,  131, 261-270.  [pdf]
Parsell, D.A., Kowal, A.S & Lindquist, S. (1994) Saccharomyces cerevisiae Hsp104 Protein. Purification and Characterization of ATP-Induced Structural Changes. J. Biol. Chem.,  269, 4480-4467. [pdf]
Storer, A.C. & Cornish-Bowden, A. (1976) Concentration of MgATP2- and Other Ions in Solution. Calculation Of the True Concentrations of Species Present in
Mixtures of Associating Ions. Biochemical Journal 159, 1-5 [pdf]

Some very good ideas, thank you! Another interesting thing I forgot to mention, is that I found evidence of substrate inhibiton of C. albicans at about 1mM ATP concentration. Perhaps this would add some valuable knowledge to the evolutionary relationship between these orthologs?

+1, I've read a few of your answers now, and I've gotta say that I'm pretty impressed. Always logical, straight-forward, complete, and referenced. Great to have you in the community :)

Me too. Personally (no maths...) impressed by "magnesium", by the way. Maybe interestingly, I would have very strictly stung to the formulation of the question: it's about one and the same protein, and including all it's properties, and that might include one and the same way to react to different concentrations of magnesium. Now I see what makes a very bad mathematician out of me - to put one and the same into a different context surely does not change that one and the same thing as such. Thank you!


text:
Advantages of gregarious vs solitary behaviour?
I'm trying to explain why birds (specifically wildfowl) are gregarious during the winter and solitary during the summer.
I think that in winter, birds are gregarious to reduce the risk of predation and to share foraging information. But gregariousness also brings with it competition, and because birds have offspring to feed in the summer, they trade-off increased predation/loss of information with reduced competition.
Does this sound correct?

what kind of effort did you put in answering yourself? have you asked google, e.g. "what are benefits of solitary in animals?"

You should add more information about your study species (living environments, migration, breeding behaviour  etc).

Question edited (hopefully improved)

sorry,. OP, it is still not good. Proper way to ask that might be something like that: "I wonder what is difference between X and Y. My hypothesis is Z, based on references A,B,C, and wild speculation D. Are there other theories?" Try to put it using as short sentences as possible and you will find help. This is not site for seeking assistance in editing writings

Another shot...

I will assume that you are talking about Mallards, although other wildfowl are likely to exhibit similar behaviors.
Mallards aren't actually solitary during the summer, instead they form breeding pairs.  They form groups (sords) in the winter to migrate and for protection while moulting.
https://sta.uwi.edu/fst/lifesciences/documents/Anas_platyrhynchos.pdf
http://thefarmatwalnutcreek.com/Ducks_Swans_Mallard-Duck.html


text:
How do birds influence brood sex ratios?
This paper concludes that birds can adaptively modulate brood sex ratios. How do birds modulate brood sex ratios? Are they somehow able to influence the sex of their young? Or once young are born, do they provision one sex with more food so that the other sex does not survive?

On a more general level it is possible for parents to influence sex-ratio of broods in a number of ways, and there are other reasons why a brood might have a sex ratio distortion. The paper I've been reading this morning is about side-blotched lizards doing just this. I'll give a quick basic answer just from the top of my head and hopefully someone can give some specific examples in birds.
Bias in gamete production
Assuming XY chromosome systems where the males are heterogametic (XY, females XX) the male can influence the brood sex ratio by producing more or less Y-bearing sperm. Sperm carrying an X-chromosome will always produce daughters and sperm carrying a Y- will always produce sons. The opposite would be true for ZZ/ZW where female gamete type determines the sex, they could only produce Z eggs, therefore only having sons.
Female cryptic sperm choice
A fairly modern idea is that females can selectively fertilise eggs with sperm based on the DNA they carry, this could include whether the sperm is Y- or X-bearing. This idea is thought to explain how females produce daughters from small sires and sons from large sires in the paper I mentioned at the start.
Meiotic drive and sex ratio distorters
Meiotic drive elements may be responsible for sex-ratio distortion in broods. Just like the biased sperm production this can alter the sex-ratio at the gamete level. Genetic effects mean that fewer offspring of one sex than the other are produced. Here is one example where suppressors of the distorter have evolved in the autosomes.
Direct selection by the parents
In the paper you mention above, and with most studies, it is possible that the parents are selecting which offspring to raise after they hatch (or as an egg - it may be possible to determine sex at that point) and if females are more costly to raise and conditions are poor, they may kill/neglect the female offspring early on.
Within brood competition
If one sex is stronger as a chick it possible that the broods could become sex biased in certain conditions which consistently favour one over the other.
Consequence of environmental strain
Similarly to the last two points, if conditions are poor it may be harder for one sex to reach maturity than the other which would result in sex-bias. This is the conclusion the authors in your paper seem to come to.
Environmental effects
As with some reptiles, environment can determine the sex of the offspring. For example, incubation temperature in turtles has a considerable effect on offspring sex ratio. Given how close birds and reptiles are in evolutionary time, and the importance of active incubation in birds, I don't see that it's impossible for the parent to vary some kind of environmental factor in order to bias sex-ratio.
There are certainly more potential mechanisms and some of these ideas are fairly new in evolutionary biology research so there are many unanswered questions. I hope I will have time to find some bird specific examples later.

Sperm production bias will, of course, not work in birds since they have a ZW sex chromosome system, not XY. I suppose the female might be able to similarly bias ovum production, though.

Thanks @IlmariKaronen - I've clarified the answer a little bit. You are of course right, I was just putting in an answer for general brood sex ratio manipulation so forgot to add the ZW specifics.

authors: Светодиодные решения


text:
List of non-native terrestrial molluscs in California?
I'm looking for a list of non-native terrestrial molluscs in California. Ideally, I also need the date each taxon was introduced into California. Can anyone help?

This might be a start: Wikipedia: List of invasive species in North America: Mollusks.


text:
What are the consequences of voluntary total celibacy?
Psychologically this might be a tough question, but in means of biology, what are the effects of total celibacy on the gonads and the nervous system concerning both man and woman in short and long term? Has there any research made in medical terms and as a bonus question, is there anything similar on other animal kingdom like deliberate celibacy?

What kinds of effects are you asking about? Changes in hormones, nervous system, organs,...?

Good point. Any effects known are on my interest. Do you think it is too wide topic then?

Possibly... most of all though I can't really imagine how celibacy would have any effect on the body apart from the brain :)

Well as far as I know, testicles are producing spermatogenesis all the time for men. What happens to that in normal sexual life compared to celibatic life for example. Maybe effects reaches also brain. I suppose there must be some implications on body.

You could rephrase the question to "effects on the gonads and the nervous system" in that case, though I'm not sure there would be any effect at all. Gonads don't normally become deficient from not being used as far as I know.

Made the change. I'd also like to know, if there is any mechanism, that actually "forces" men or why not men too to ejaculate, like for a reason to clean or refresh gonads or is this done by normal body's metabolism. And if there are any harm that celibacy could do in terms of biology. All this could be handled on answer.

I was told in my undergraduate degree that males produce sperm all the time, and that under conditions of no sexual stimulation, that sperm is excreted involuntarily every 15-16 days, at night, while dreaming. I was also told that the renewal rate of sperm is higher under regular sexual stimulation, which increases the fertility of the sperm that is excreted.

This is very interesting if true. It means that for thousands of years, monks and other ascetics who abstain from sex/masturbation have still been having fairly regular ejaculations, making the whole thing much more bearable. I always thought it seemed an inhuman feat!

If there is any research papers on public, I'd like to see them. I also happen to have opportunity to ask this question from several decades being Indian brahmacarya meaning celibate monk in few days I think. Let's see how it correlates with teachings on schools. Also this is male specific, is there counter part for similar organ behavior for females?

@Richard “monks and other ascetics” – note that the former doesn’t imply the latter. I’m suspecting that the representation of monks in The Name of the Rose is more than a little true, both now and then.

@PHPGAE: it is what is usually called a wet dream. The scientific name is Nocturnal emission and it happens in both sexes.

Site says, involuntary excretion cycle was averaged from three weeks to 5,5 weeks. High testosterone increased cycle, supposedly low testosterone decreases the cycle. Depending on that and age natural emission occurs for celibates, which can be also interpreted, that there is nothing unnatural on celibacy, because nature handles things anyway. However Indian yogi I met today said, that normally it happens about once per month if energy is not cultivated by psycho-physical exercises. He claimed full-time monks can be without ejaculating months after months, years after years no problem.

So I cannot accept the answer from that part because cycle is inaccurate and it seems there are exceptions on "law".

@KonradRudolph you're right, perhaps just "ascetics". I don't want to make any claims about the behaviour of monks...

I'm not sure how to proceed with this topic, but I made a voluntary experiment past year and decided to have a full celibate. I countered only one nocturnal flow, I should say partial, between whole 365 day test period. I think there a lot to research on this topic on academic circles. I could collect some thoughts and observations from memory, but they would be totally personal and might not help from empiric view of point. I wonder if there are peer groups, that could collect information by interviews or similar and give scientifically & statistically more interesting data...

Not entirely on your question but I think sufficiently relevant:
This paper (freely available) identified a non-causal link between ejaculatory frequency and incidence of prostate cancer.

Men were asked their age at first ejaculation, the maximum number of ejaculations ever experienced in 24 h, and to estimate the average number of times that they had ejaculated per week in their most sexually active year in each of three decades of age (i.e. third, fourth and fifth).

Leading to results indicating that:

Greater ejaculatory frequency in the most sexually active year in each of the three decades was associated with a significantly lower risk, with men in the upper quartile of ejaculatory frequency having about two-thirds the risk of those in the lower quartile for the third and fourth decade, and four-fifths the risk for the fifth. Ejaculatory frequencies in each of the decades were correlated with one another (r = 0.5–0.7). A similar finding related to the total number of ejaculations over the three decades. Those who reported an average of four to five or more ejaculations per week had two-thirds the risk compared with those who, on average, ejaculated less than three times per week.

Giles, G.G., Severi, G., English, D.R., McCredie, M.R.E., Borland, R., Boyle, P. and Hopper, J.L. (2003), Sexual factors and prostate cancer. BJU International, 92: 211–216. doi: 10.1046/j.1464-410X.2003.04319.x

This was worth of mentioning I think.


text:
Does every person have unique nervous system?
If we had the technology to directly interface electronic devices with the nervous system and we wanted to connect a robotic arm to a person that lost his/her real arm, would we be able to find the same "wires" that control(led) that arm in every person?
Or does every human control their organs in completely unique, "incompatible" way?

Probably the best way to answer this question is with a counterexample to humans: the nematode worm C. elegans has 302 neurons. Every individual has exactly that number, and each is found in the same place with the same function in every individual. This is one of the things that makes C. elegans an attractive model organism for study.
Humans definitely do not develop the same way. There are certainly groups of neurons that are found in every individual, and many of the tracts have at least a typical anatomical course that can be found from individual to individual, but it's not as if you can arrange each of the tens of billions of neurons in a list and find the same "Neuron #10,934,035,587" in two different people.
The most successful prosthetic operation that interfaces with the neuromuscular system these days is through myoelectric control, where rather than using electrical activity from neurons, one uses electrical activity in muscles, such as muscles in the chest and shoulder to control a prosthetic arm or hand.

But when they do things like hand transplants, they connect the patient's nerves to the nerves in the transplanted limb, don't they? People are similar enough for this to be feasible.

@Barmar They can connect nerves, but not neurons. The individual neurons need to re-grow through the nerve structure. "Re-wiring" the hand from that point onward is a result of extensive physical therapy and more about plasticity in the CNS than rewiring in the periphery. A similar process would happen if a nerve were severed and reattached in the same patient without a transplant; it's also somewhat similar to how those connections are developed in the first place. Human infants are born with fairly incomplete motor control and so are an (adorable) excellent insight into this.

The OP didn't specify individual neurons. I think his figurative "wires" equates to nerves.

(it's also worth noting that a lot of hand control occurs outside the hand)

@Barmar That's possible, but then you'd have to also specify the detail of nerve. Everyone has a spinal cord where nerves leave at every vertebral level, sure; from there, variation increases the more distal you get. Hooking things up at the nerve level isn't sufficient to connect electrical devices to the nervous system; the only way to do it is to let the nervous system learn associations with the connections you've made. Every attempted brain-machine-interface or nerve-machine-interface has done this.

My thinking is that the details are unique like fingerprints, but at a higher level it's similar like the general structure of fingers.

@Barmar Sure, but isn't it a bit superficially obvious that if you have a finger, it has to have nervous innervation? "People have fingers" is enough to tell you that; the interesting part would be considering whether there is some one-to-one relationship between the neurons and structure of the finer nerve endings in two people; there isn't.

I guess what I'm saying is that the arteries and veins have direct correspondences that allow you to connect these, and there would be similar correspondences for nerves. There will be minute differences, but not enough to prevent reconnection.

@Barmar Only at a very gross level. For example see this question: https://biology.stackexchange.com/questions/82918/coronary-circulation/ about a common difference in the coronary circulation, and that's in a couple of major vessels together supplying over half of the blood to the heart. Have a look at the superficial veins in your arm that are quite visible from the surface: you'll find they vary quite a lot.

agreed yes you can connect the same nerves but neuron to neuron will be slightly different, especially in the brain, but the person can learn to control the new limb without problem it will just take time.  translpantees will have gross control fairly quickly but precision control takes a long time.

WRT C. elegans, neurons are actually a fairly high level of nervous system organization.  Neurons have many dendrites (IIRC something like 1-10K branches in humans) & many synapses whose state changes due to synaptic plasticity.  And researchers keep finding more low-level complexity: https://www.quantamagazine.org/neural-dendrites-reveal-their-computational-power-20200114/


text:
Is collagen supplementation useless?
When collagen is digested is it broken up into usable components that the body can use to produce its own collagen?
What evidence is there that supplementing with collagen type I & II etc.. can help connective tissue disorders?
What evidence is there that supplementing with collagen from animal products is not useful?

I don't see a reason why collagen should be digested differently from other proteins. It is broken down into amino acids. And of course they can be used to synthesise collagen if needed. I can't answer whether dietary supplements have been proven useful/less though.

Also note that the aminoacids that make up collagen are not special. They can be used by the body to make up any other protein.

We may want to put this on skeptics.se Let's see what response come here first.

Regarding the use of collagen supplements to help prevent or treat a tendinopathy:
A rather inconclusive quote from a 2016  systematic review {1}:

glucosamine and chondroitin sulphate, vitamin C, hydrolazed type 1 collagen, arginine alpha-keto-glutarate, bromelain, curcumin, boswellic acid, and methil-sulfonil-methane were considered […]. preclinical results are very encouraging, however they are not fully confirmed by clinical studies. There are few clinical papers on the use of nutraceuticals in tendon disorders, and their methodological quality is poor. Furthermore, in most of the studies more than one supplement was administered at the same time. This may bias the results, and the effect of each single component cannot be determined. Furthermore, the interactions between nutraceuticals and drugs, or other dietary supplements (especially at high doses) has not been evaluated, neither their effects on chronic diseases. For these reasons, it is not possible to draw any definitive recommendations on the use of nutraceutical supplementation in tendinopathies.

References:

{1} Federico Fusini, Salvatore Bisicchia, Carlo Bottegoni, Antonio Gigante,3 Fabio Zanchini, and Alberto Busilacchi. Nutraceutical supplement in the management of tendinopathies: a systematic review. Muscles Ligaments Tendons J. 2016 Jan-Mar; 6(1): 48–57. Published online 2016 May 19. doi:  [10.11138/mltj/2016.6.1.048] PMCID: PMC4915461. PMID: 27331031. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4915461/

This seems to be an interesting and ambiguous topic.
On one hand, the collagen as any other protein is cleaved into small-sized chunks (oligopeptides) and single aminoacids before absorption. The chunks of proteins which were not completely digested before absorption are broken up further in the body and cannot be selectively used for collagen re-building in the body. Therefore, there should be no difference between the collagen of different types and, basically, no difference between the supplements containing collagen and just a mixture of aminoacids. This also explains the fact why collagen supplement is in most cases taken in the lysate (pre-cleaved) form.
On the other hand, a quick search in PubMed and I found an interesting article on the topic (source), where the authors claim:

At 6 months, the proportion of clinical responders to the treatment,
  according to VAS scores, was significantly higher in the collagen
  hydrolysate (CH) group 51.6%, compared to the placebo group 36.5%
  (p<0.05).
...
This study suggests that collagen hydrolysate 1200 mg/day could
  increase the number of clinical responders (i.e. improvement of at
  least 20% on the VAS) compared to placebo. More studies are needed to
  confirm the clinical interest of this food supplement.

So, if the article is not a bogus (I failed to get the full version of it and the journal does not seem to belong to the top journal in the field of medicine), there could be some mechanisms yet to be discovered.

I guess it may be a result of the fact that CH has a very high % of Gly and Pro, more than what you would normally get from food. Wikipedia lists several studies that have given widely discordant results on the matter of whether it helps with joint diseases.


text:
Can NSAIDs impact negatively the healing of tendons?
There are a number of articles regarding nonsteroidal anti-inflammatory drugs
 (NSAIDs) having a negative effect on healing conditions like tendonosis and tendinitis. From what I understand the channel through which they reduce inflammation disrupts healing. In general, many of them constrict vessels, thus reducing bloodflow even further to tendons. Are there other reasons, or interactions they can have with  cells that may also disrupt healing?
Are there advantages of using NSAIDs to promote healing?

I would suggest you contact your doctor if you are suffering from tendinitis.
NSAIDs are often used as part of treament for tendinitis, but like all medications they can have side effects. Therefore again if you have concerns about taking NSAIDs contact your doctor.
As for the mechinism of action of NSAIDs they don't constrict vessels but instead reduce the production of inflammatory mediators (prostoglandins) which act to dilate some vessels. These inflammatory mediators also make blood vessels more permeable so that nutrients and cells from the blood can pass through the vessel walls and carry out repairs to damage tissue. The problem however with the bodies inflammatory response is that it can be too severe, so that rather than providing healing it itself can cause damage and pain. For this reason (and many others) NSAIDs may be useful.
But again if you have concerns about taking NSAIDs or any medical condition these please consult your doctor. The internet is not an appropriate place for medical advice, your doctor is.

"But again if you have concerns about taking NSAIDs or any medical condition these please consult your doctor. The internet is not an appropriate place for medical advice, your doctor is." -> the internet is a perfectly fine place for medical advice and can be a great source of information in addition to a 15-minute appointment with a physician.

As far as I know there is no clear scientific evidence on whether and at which stage of a tendon injury one should use NSAID. Here is the conclusion of a systematic review from Cochrane {1}:

There remains limited evidence from which to draw firm conclusions about the benefits or harms of topical or oral NSAIDs in treating lateral elbow pain. Although data from five placebo-controlled trials suggest that topical NSAIDs may be beneficial in improving pain (for up to 4 weeks), non-normal distribution of data and other methodological issues precluded firm conclusions. Some people may expect a mild transient skin rash. Evidence about the benefits of oral NSAIDs has been conflicting, although oral NSAID use may result in gastrointestinal adverse effects in some people. No direct comparisons between oral and topical NSAIDs were available. Some trials demonstrated greater benefit from glucocorticoid injection than from NSAIDs in the short term, but this was not apparent in all studies and was not apparent by 6 months in the only study that included longer-term outcomes.

Some papers argue that the inflammation has a positive action on the tendon repair whereas some other papers claim the contrary. Given the current state of tendon injury research, it's not even clear how much inflammation happens during a tendinopathy {2,3,5}. From {4}:

FYI:

Do nonsteroidal anti-inflammatory drugs (NSAIDs) decrease or increase swelling during the acute phase of a tendon injury?
What is the proper timing for dexamethasone injections to improve the healing of damaged tendons in humans?

References:

{1} Pattanittum P, Turner T, Green S, Buchbinder R. Non-steroidal anti-inflammatory drugs (NSAIDs) for treating lateral elbow pain in adults. Cochrane Database of Systematic Reviews 2013, Issue 5. Art. No.: CD003686. DOI: https://dx.doi.org/10.1002/14651858.CD003686.pub2
{2} Rees, Jonathan D., Matthew Stride, and Alex Scott. "Tendons–time to revisit inflammation." Br J Sports Med 48, no. 21 (2014): 1553-1557. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4215290/ ; https://dx.doi.org/10.1136%2Fbjsports-2012-091957
{3} Khan, Karim M., Jill L. Cook, P. Kannus, Nicola Maffulli, and S. F. Bonar. "Time to abandon the “tendinitis” myth: painful, overuse tendon conditions have a non-inflammatory pathology." (2002): 626-627. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1122566/ ; https://dx.doi.org/10.1136%2Fbmj.324.7338.626
{4} https://youtu.be/z_QJYDgO6yQ?t=1129 "History and future of tendinopathy"
Sports Medicine Congress 2016. Comwell Hotel, Kolding - 04-06 February 2016. Follow the conference at twitter @sportskongres or #sportskongres
{5} Mosca, Michael. "Re-evaluating tendon disease: an emerging role for inflammation and alarmins." Master Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:360eb093-9a3b-4271-a5b6-31314c7e1bbd ;  (Google Scholar) (mirror)


text:
What are tendons made of specifically
From what I read on wikipedia they are made of collagen. Collagen is just a protein. Right? How is this collagen structured (I imagine like fibers). Aren't there cells in this fibers as well?
From this picture:

Is the pink stuff the collagen? and the purple stuff the tenocytes?
If someone can expand on this with a picture preferably, it would be great.

As you correctly say, tendons are made up of collagen fibers. Collagen is one of the most important proteins (or, to be more specific, family of proteins, as there are many types of collagen) forming connective tissue in the body.
Collagen molecules have a particular structure that allows them to form long fibers, composed by three different strands that form a triple helix. This is a schema of a collagen helix (each ball represents one aminoacid):

(source: Wikipedia)
These helices can then be bound together to form a collagen fiber, through the action of an enzyme called lysyl oxidase which binds two lysine residues from two different helices together (lysine is one of the aminoacids that makes up collagen).
Here is a scanning electron microscope of a collagen fiber:

(source: Science photo library)
Collagen is secreted out of the cells that produce it so, although there may be cells around the collagen molecules, it is important to understand that it is part of what is called the extracellular matrix, the extracellular structure that supports the cells in our body.
As for the photo you linked, it is an hematoxylin and eosin (H&E) stain of a tendon. Hematoxylin colours cell nuclei in dark blue, so the dark spots are definitely cells.
The pink "waves" are indeed collagen fibers, the cells are probably the tenocytes, the specialized fibroblasts of the tendon, which produce the collagen.

Do these tenocytes move around the collagen fibers? Sort of like spiders in a web?

@user952: I don't really know. I would say no, but I may be wrong.

@user952 tenocytes can move: What causes tenocytes to migrate from intact regions of tendon into the wound site, and how do they move?

also Do tenocytes move around in a healthy tendon or do they stay at the same location?

{4} has a similar micrograph as yours but with some labels:

with the caption:

Figure 1.2: Tendon microstructure of healthy tendons: nuclei of tenocytes are darker in color and vascularization does not disrupt collagen arrays.  arrays
  http://www.onlineveterinaryanatomy.net/content/tendon-histology-labelled (mirror)

{5} presents both a longitudinal (a) and a transversal view (b):

Caption:

(a) A low power, longitudinal section through the limb tendon of a young calf in a section stained with Haematoxylin and Eosin (H & E). The tenocytes (TC) are typically arranged in longitudinal rows between parallel bundles of collagen fibres (CF) and are only recognizable in such routine sections by their darkly staining nuclei (i.e. the cytoplasm is not visible). Note the waviness (crimp) of the collagen. (b) A low power transverse section through the limb tendon of a young calf stained with H & E. Note that the collagen fibres are grouped into fascicles (FA) separated by endotenon (E). The tenocytes are recognizable within the fascicles by their nuclei (arrows).

Some illustrations showing the tendon structure:

(image source) (mirror)

(image source) (mirror)
Another illustration from {3}:

Regarding the cellular content of tendons, quote from {1}

The cellular content of tendons accounts for 20% of the overall tissue volume (Nordin et al., 2001). The main cell type present within tendons, which is responsible for the production and regulation of ECM, is the tenocyte (Maffulli et al., 2002). These are bipolar cells with elongated nuclei and spindle-shaped morphologies; they are regularly anchored in columns amongst the collagen bundles (Bernard-Beaubois et al., 1997). Other cells (though present in smaller numbers) include chondrocytes present at OTJ insertion sites, synovial cells composing the tendon sheath and vascular cells such as capillary endothelial and arteriole smooth muscle cells (Sharma and Maffulli, 2005).

Some more details from {2}:

The matrix is far more conspicuous than the cells. However, it is now widely recognised that the cellular elements hold the key to understanding development, repair and the ability of tendons and ligaments to respond to changing mechanical load. Tenocytes are mechanosensitive cells that are hardwired in a way that allows them to deploy a tensegrity architectural system to detect changes in mechanical load via deformation of their cell membrane and cytoskeleton (Wang, 2006). Strain in the extracellular matrix (ECM) tenses cytoskeletal fibres via integrin receptors in the cell membrane, and this in turn is relayed to the cell nucleus so that gene expression can be altered. An important principle of the tensegrity system is fibre continuity between the ECM and the cells. As Myers et al. (2007) point out, the implication is that the existence of a continuous network of fibres (i.e. collagen fibres in the ECM; cytoskeletal fibres in the cells) means that stress on one part of one cell can be dissipated throughout the entire tissue. Consequently, individual cells are protected from damage and a small mechanical stimulus can potentially affect many cells (Ingber, 1997; Myers et al., 2007). It is also worth noting that an under-stimulation of tenocytes that results from an altered cell–ECM interaction consequent upon tendinopathy could down-regulate cell activity (Arnoczky et al., 2007). Thus, the tendon becomes weakened and more vulnerable to damage from mechanical overload.
Although tenocytes and ligament fibroblasts are unremarkable cells in routine histological preparations and seemingly isolated within the ECM (Figs 14.2 and 14.3), they have a much more elaborate form when viewed by confocal microscopy (McNeilly et al., 1996). Each cell has numerous finger-like and sheet-like processes, extending around groups of collagen fibres and creating a 3D network of intercellular contacts throughout the tissue that fits well with the tensegrity model discussed above. The tenocytes are typically arranged in longitudinal rows, where the long axis is parallel to the tendon itself (Fig. 14.3). This reduces the risk of cell damage accompanying tendon or ligament loading. Adjacent cells communicate with each other via gap junctions – structures that allow ions and small molecules to be rapidly exchanged between individual cells. Two types of gap junctions are present in tendons – those expressing the protein connexin (cxn) 32 and those expressing cxn 43 (McNeilly et al., 1996; Ralphs et al., 1998). It is notable that the distribution of these two connexins is distinctive and implies they have independent functions. Connexin 32 is only present between cells within a longitudinal row, whereas cxn 43 also links cells in adjacent rows. Consequently, gap junctions containing cxn 32 are oriented along the line of tensile loading of a tendon, but cxn 43 junctions link cells in all directions. Waggett et al. (2006) have since shown that collagen synthesis is inhibited in avian tendon cells subject to cyclic mechanical loading in vitro, via cxn 43 and stimulated via cxn 32. Thus, it seems likely that the interplay between these junctions in response to load changes in tendons and ligament is critical in allowing them to adapt their ECM to changing mechanical load (Waggett et al., 2006). The integrity of the cell junctions in a compliant tendon seems to be ensured by the presence of longitudinally oriented, actin stress fibres within the tenocytes, which are associated with adherens junctions that link cells within the same longitudinal row (Ralphs et al., 2002).

For more details on tendon structure, see {5,6}.

References:

{1} L.A. Bosworth, in Electrospinning for Tissue Regeneration, 2011. https://www.sciencedirect.com/book/9781845697419/electrospinning-for-tissue-regeneration ; The quote I took came from https://www.sciencedirect.com/topics/engineering/tenocytes (mirror)
{2} M. Benjamin, in Regenerative Medicine and Biomaterials for the Repair of Connective Tissues, 2010. https://www.sciencedirect.com/book/9781845694173/regenerative-medicine-and-biomaterials-for-the-repair-of-connective-tissues ; The quote I took came from https://www.sciencedirect.com/topics/engineering/tenocytes (mirror)
{3} Docheva, Denitsa, Sebastian A. Mueller, Martin Majewski, and Christopher H. Evans. "Biologics for tendon repair." Advanced drug delivery reviews 84 (2015): 222-239. https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Biologics+for+tendon+repair&btnG= ; https://doi.org/10.1016/j.addr.2014.11.015
{4} Mosca, Michael. "Re-evaluating tendon disease: an emerging role for inflammation and alarmins." Master Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:360eb093-9a3b-4271-a5b6-31314c7e1bbd ;  (Google Scholar) (mirror)
{5} Benjamin, M., E. Kaiser, and S. Milz. "Structure‐function relationships in tendons: a review." Journal of anatomy 212, no. 3 (2008): 211-228.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408985/ ; https://dx.doi.org/10.1111%2Fj.1469-7580.2008.00864.x
{6} Lavagnino M, Wall ME, Little D, Banes AJ, Guilak F, Arnoczky SP. Tendon mechanobiology: Current knowledge and future research opportunities. J Orthop Res. 2015;33(6):813–822. doi:10.1002/jor.22871 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4524513/; https://dx.doi.org/10.1002%2Fjor.22871


text:
Which cells are responsible for the extracellular matrix remodeling?
I am studying a case of tendinopathies induced by an alteration of how the extracellular matrix is being remodeled.
From my understanding there has to be a careful balance of MMP (metallproteinases) and TIMP enzymes to maintain tendon homeostasis.
Which cells produce these enzymes?

Taken from The role of matrix metalloproteinases (MMPs) in the pathophysiology of chronic obstructive pulmonary disease

Metalloelastase (MMP-12) is (as the name suggests) capable of
  degrading elastin, as well as other extra-cellular matrix components.
  It is produced predominantly by infiltrating macrophages and appears
  essential for macrophage migration through extra-cellular matrix

Matrix Metalloproteinases in Cancer Cell Invasion gives a more thorough description of the various MMP and TIMP types

MMPs are mainly produced by nonmalignant stromal cells in malignant
  tumors. Tumor cells also secrete factors, such as extracellular MMP
  inducer (EMMPRIN), which enhance the expression of MMPs by stromal
  fibroblasts (see Toole, in this book). In addition, growth factors and
  cytokines secreted by tumor-infiltrating inflammatory cells as well as
  by tumor or stromal cells modulate MMP expression.

Thanks for your input... I am trying to understand how Fluoroquinolone drugs can degrade tendons. From what I am understand MMP-9 is of my concern:
"Our study provides preliminary evidence that topical application of fluoroquinolone drugs can induce the expression of MMP-1, MMP-2, MMP-8 and MMP-9 in the undebrided corneal epithelium compared to artificial tear eye drops." (http://www.ncbi.nlm.nih.gov/books/NBK6598/)

Here's another one:
http://www.wikigenes.org/e/ref/e/12428247.html
Ciprofloxacin enhances the stimulation of matrix metalloproteinase 3 expression by interleukin-1beta in human tendon-derived cells. A potential mechanism of fluoroquinolone-induced tendinopathy.


text:
How fast does the rotor in ATP synthase spin?
I'm sure the exact frequency varies, but does anyone know roughly how many revolutions per minute / second the rotating center part makes?

According to "Resolution of distinct rotational substeps by submillisecond kinetic analysis of F1-ATPase" (Yasuda et al., Nature, 2001), ATPase rotates at 130 revolutions per second when saturated with ATP.

The rotation rates at various ATP concentrations obeyed the curve defined by a K m of ≈30 μM and a V max of ≈350 revolutions per second (21 000 revolutions per
minute) at 37°C.
Some reported values of very high ATPase activities would predictrapid rotations such as bovine mitochondrial F1 (≈310 rps) (37), yeast mitochondrial F1 (≈280 rps) (38), and E. coli FoF1 (≈300 rps) (39). Much lower ATPase activities corresponding to 10 ≈ 100 rps were also reported in many papers. However, if a significant fraction of  molecules in the bulk solution are in the ADP-Mg-inhibited state or other inactive states, as in the case of thermophilic FoF1, real ATPase activity specific for the working enzymes should be higher, and the rotation rates can be much faster. It is intriguing to learn whether these rapid rotations are really occurring in living cells.

These are excerpts from:
Ueno, H., Suzuki, T., Kinosita, K., & Yoshida, M. (2005). ATP-driven stepwise rotation of FoF1-ATP synthase. Proceedings of the National Academy of Sciences, 102(5), 1333-1338.
.

Welcome to Biology.SE! In the future please include full reference information for papers rather than just a link — this is because links can break (as can be seen in the previous answer). ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. In particular, it would make a more effective answer if you were to summarize the results from this paper rather than just copying text (including reference numbers that have no context). Thanks!


text:
Is there a comprehensive database of fossils (with images) online?
Not sure if this is the best stackexchange to ask...
I have not been able to find a decent database of fossils on the web, does one exist?
Here are some of the links I have found through Wikipedia and Google:

http://www.paleoportal.org/index.php?globalnav=doing_paleo&sectionnav=more_submissions&state_id=0&submission_type_id=27&type_id=5
http://www.morphobank.org/index.php/Projects/Index
http://research.amnh.org/paleontology/
http://en.wikipedia.org/wiki/List_of_fossil_sites
http://www.fossilsites.com/STATES/AB.HTM
http://inyo.coffeecup.com/site/ammonoids/ammonoids.html
http://www.historicalclimatology.com/
http://geonames.usgs.gov/pls/gnispublic/f?p=gnispq:3:4473291015495555::NO::P3_FID:354414
http://www.scotese.com/earth.htm
http://www.trilobites.info/biostratigraphy.htm
http://burgess-shale.rom.on.ca/en/
http://www.fossilmuseum.net/FossilGalleries.htm
http://www.kumip.ku.edu/cambrianlife/Utah-Online-Fossil-Exhibits&Collections.html
http://www.ucmp.berkeley.edu/collections/catalogs.html
http://peabody.yale.edu/collections/search-collections?vp
http://books.google.com/books?id=Ezm1OA_s6isC&printsec=frontcover&dq=hartwig+primate&cd=1&hl=en#v=onepage&q&f=false

What are the best places to get fossil data and images of the fossils? Or are museums and textbooks the only alternative?

If you already found some sites that fit the bill, they may be better off posted as an answer. Per the [FAQ#dontask]: avoid asking subjective questions where... your answer is provided along with the question, and you expect more answers: "I use ______ for ______, what do you use?".

What are you looking for that these sites lack?

paleodb.org seems to have a huge database linking fossil records to publications. But it is not clear what you want, nor is it clear why the 16 pages you listed are insufficient. If you clarify that I am sure someone will be more able to help.

there are a few places trying to create a comprehensive list, but most of those are still specialized towards things like vertebrates or pollen. the morphbank in particular want to not only create a list but also include all  relationship studies in a single searchable index.  Adam gives a good reason why these take so much time and effort to create.

http://tolweb.org/ can at least give you names.

note that  publication descriptions of a fossils are required to provide a repository, a location the fossil can found at. this is why a common database has bot been a big issue until recently, a researcher would know where all the relevant material could be found. In paleo many comparisons are still done by traveling to the place and looking at the fossils side by side. I have been to museums were the only database of their specimens was a card catalog.

No. Museums are the traditional repository for fossils, and the process of "digitizing" their collections is slow and labor intensive. Often, the museums only aim to digitize what me might call the "meta-data" associated with the fossil, as was done here:
http://ucmpdb.berkeley.edu/cgi/ucmp_query2?admin=&query_src=ucmp_index&table=ucmp2&spec_id=V8111&one=T
A truly comprehensive database is not feasible in the near future. A single photograph likely would not be sufficient to characterize the fossil -- the interesting components of fossils are often microscopic. For example:
http://www.pnas.org/content/99/14/9117.full.pdf
Even taking a single photograph can be very labor intensive, and fossils can be fragile. Proper photo-documentation would probably require multiple images. More generally, a comprehensive database would probably need to include non-photographic data relating to the fossil -- such as chemical composition of non-visual imaging techniques (X-ray, IR, UV, etc).
For the foreseeable future, "comprehensive" collections will be housed in museums without full digital representation. The only way to know how comprehensive these collections are is to ask the museum curator, who will be aware of the scope and limitations of the collection.


text:
Why is the  microbial ecosystem of the gut so susceptible to disruption by pathogens?
From all accounts, it seems as if the Escherichia, Enterobacter, etc. that live and thrive in the human gut are pretty well entrenched.  I know that these microbial populations are often analyzed as an ecosystem.
What surprises me is that it seems like minor food poisoning can throw the whole ecosystem off.  I know superficially that Clostridium are contenders in the fight because they remain viable after traveling through the acid of the stomach, but why are these populations so sensitive to other invading bacteria?

Hi! Could you please give some references to the fact that minor food poisoning can throw the whole ecosystem off? This is very interesting to me, as a personal health matter.

@dignor.sign I was more making an observation, but see http://en.wikipedia.org/wiki/Gut_flora#Alterations_in_flora_balance, A reduction in levels of native bacterial species also disrupts their ability to inhibit the growth of harmful species. They cite 3 references, including a Lancet article, but say that this may in fact not be the cause of symptoms such as diarrhea (apologies for the graphic description).

I was just curious about how weak this ecosystem can be; these papers will do it. Thanks!

Keep in mind one of the most common harmful species is a native species in many people: Clostridium difficile.

@EpiGrad Excellent point.  If your up for it, elaborate it a bit as an answer.  I don't know much about how it achieves balance with E. coli.

I would actually disagree with the whole idea that the bacterial community in the gut are very susceptible to disruptions. Imagine how many different potential pathogens we ingest every day, and how often do we actually show symptoms?

@Zewz Overall, I would certainly agree, but I've seen otherwise healthy people reduced to nothing over what started as a minor Clostridium sp infection.  Certainly, if you want to elaborate on this point, I'd always welcome another answer on the question.

There are two types of food poisoning:
Alimentary intoxication
This is the case when you consume food which is contaminated with some toxins, and those are responsible for development of the poisoning symptoms. The source organisms of these toxins might not be present anymore (killed by heating during cooking, for example). In this case there is no massive invasion of any foreign organisms into the gut.
Alimentary toxico-infection
This happens if you eat the food contaminated with microorganisms, and these start to massively proliferate in your alimentary system causing the symptoms of poisoning. The massive intake of the bacteria (even 2-3 spoons of contaminated food might contain millions of bacteria, like Staphilococcus in contaminated diary products). In this case the balance of gut microflora is dramatically changed due to introduction of a considerable amount of foreign microorganisms.
So, even the poisoning seems to be "minor" (e.g., its symptoms are not so dramatic), there could be different amounts of bacteria invading the guts.
The second important point here is the increased emptying of the gut due to diarrhea that leads to the washing out some of the "good" bacteria from the guts, especially in case of profuse diarrhea. The newly coming bacteria are not necessarily those that are present in normal microflora, and it takes days or even weeks until the microflora reaches homeostasis again.
One last point: even without poisoning, microflora varies, and the amount of different bacterial fractions can fluctuate over time. This is normal and depends upon your eating habits, your environment, immune status, and many other factors.

As requested, elaborating this into a full answer.
Three things to consider:

"Alterations to gut microflora" need not only be the invasion of a different, aggressive species of bacteria. One of the most common, and most dramatic forms of alteration to our gut flora is something we do to ourselves: antibiotics. Most ecosystems, micro or macro, are pretty vulnerable to the equivalent of a sustained firebombing.
Some of the "harmful bacteria" that benefit from a disruption of the gut microflora are constituent components of said flora. Clostridium difficile is part of the normal flora of many people - and acquired by many more transiently without incident - yet when the environment is sufficiently disrupted by antibiotics, peptic acid suppressors or some other factors, it proliferates and causes illness.
While it may feel awful to you, many GI illnesses are really just a transient invasion before the body clears the infection, and are only marginally disruptive, or not disruptive at all. This can include the intake of toxins without the actual organism, or things like norovirus, which has a low enough infectious dose that even small amounts will make you ill.


text:
Is there a binding affinity metric for interactions not in equilibria?
I am investigating the strength of binding of a small peptide to a protein by isolating the bound version and subjecting it to collisions with gas molecules (CID mass spectrometry) to dissociate the complex.
When I plot the collision energy against the proportion of bound and unbound proteins I get a curve that looks like a Kd curve.  However, as the interaction isn't in equilibria (i.e. it is in the gas phase) calculating the Kd value wouldn't be correct.
So is there another value I could calculate to describe the strength of the interaction?

Bobthejoe was pointing in the right direction  kcat and Km - Michaelis Menton parameters are measured to look at the relative rates of an enzyme in non equilibrium state.  Basically kcat is 'how fast does the enzyme work with little or no product in solution'. Km is 'how strongly does the enzyme bind the substrates that it uses.
http://www.pearsonhighered.com/mathews/ch11/c11kkkk.htm

You should be looking at the interactions in terms of kinetics and not thermodynamics. k_on and k_off should do the trick.

I don't think this is right because, k-on/k-off = Ka and Ka=1/Kd. So that would mean having K-on and K-off would allow you to calculate Kd, which is an equilibrium measurement... ah well thanks for trying!

Your basing your argument on psuedosteady state criteria and a constant concentration of your peptides and proteins. k_on and k_off are exclusively kinetic based terms that can be extended to thermodynamic terms when in equilibria which you're not in.