HeLa cells (which are of course derived from a cervical cancer) have actually been injected into humans to see if they would grow; they grew briefly but were promptly rejected. Similarly, surgeons have on occasion accidentally stabbed themselves and inoculated themselves with the human tumors they were operating on.

Injecting human cancer cells is a far greater risk than eating non-human cancers, and even in that case the risks seem to be very low.

There have been rare cases of people with profoundly suppressed immune systems (organ transplant recipients) allowing a transferred tumor to grow, so (though of course the risk there is vastly higher than merely eating a cell) it's not completely impossible.

Pragmatically, it's very likely that everyone who's eaten, say, chicken has unknowingly consumed some chicken tumors.


Plants do have uncontrolled tumorous growth. Though in almost all known cases, it is pathogen induced; such as in the case of the bacterium- Agrobacterium tumefaciens. Viruses can also induce plant tumors. Theoretically, the cell wall will pose a mechanical barrier to cell division. Also, cell wall synthesis is an extra biochemical step during cell division. Surely, the presence of a cell wall will disallow any metastasis if it might occur. There is an old article which says that cell wall structure differs between the normal plant tissue and the crown galls (tumor). However, this is with respect to Agrobacterium adsorption sites.

I am not aware of any natural plant tumor or the role of telomerase in plant tumorigenesis. However, there is one paper that says that telomerase dysfunction leads to disorganized growth.


What negative effects does cannabalism have in other species (like prion diseases) and how are they mitigated?

First, to be clear, the very act of cannibalism does not cause the development of prions, but the consumption of an animal infected with a compatible form of them, particularly when eating nervous or digestive tissue (i.e. the brain, spine, stomach, or intestines).

To directly answer your question, yes, there are other animals that are susceptible to prions diseases when they consume infected members of their own species, or members of compatible carrier species. In the late 80s and 90s, there was a moderate epidemic of Bovine Spongiform Encephalopathy (Mad Cow Disease) that was concluded to have been caused by including bovine parts in cow feeding stock.

A common defense that I know of against infection from the consumption of infected animals is to simply not consume them at all. I know it's not really the answer you were expecting, but indeed, many animals have an active aversion to corpses, notably perceiving the smell of Cadaverine and Putrescine as repulsive. Evidently, a great defense against disease is to just not eat dead or dying things.

I've never heard of insects or arthropods having neurodegenerative prions, and wasn't able to find anything alluding to them having them, but I wouldn't be too surprised if they had other prion diseases that were infectious between them.

Sources:

Matravers et al. FST (2001);17,1-19

Also available at The National Archives

Cadaverine on Wikipedia
Putrescine on Wikipedia
Sacculina on Wikipedia


What are the clotting factors' effect on avascular necrosis development?

First of all we should distinguish between the physiological clotting factors that are parts of the normal clotting pathways, and those that might affect clotting pathways but are not observed under healthy conditions.

TPA (tissue plasminogen activation), PAI-1 (plasminogen activator inhibitor) and prothrombin are normal clotting factors that are essential for blood clotting. Any deficiency (congenital or acquired) might cause certain pathologic conditions, including the osteoarthritis and avascular bone necrosis.

Lupus anticoagulant, however, is an antibody against cell membrane that is common for Lupus. This antibody can intervene into the process of clotting and increase the prothrombine time (the common lab method to test blood clotting properties), hence the name "anticoagulant". But this effect is just a sort of "side-effect" of this antibody, that leads to certain symptoms in case of auto-immune attack against different target organs.

So, after this introduction I can rephrase your first question as: "Does the deficiency of clotting factors TPA and PAI-1 lead to degenerative arthritis in the same way that lupus anticoagulant and prothrombin deficiency might?"

The part of the answer is already in this question: yes, the deficiency of these factors might and under certain conditions, leads to the development of osteoarhritis and avascular necrosis.

I must confess, I found no evidence whether the underlying mechanism is different or not. Papers just prove that these factors are discovered in the affected joins, and see the correlation in mice models between the factors and the articifially induced arthritis. But I found no study which would try to address the mechanisms of these actions or to show, whether these are different.


Do adult mammalian cochlear inner hair cells regenerate?

Short answer
The current consensus is that hair cells in the cochlea of humans do not regenerate spontaneously.
Background
I took the liberty to show the linked paper to a colleague of mine. This guy has been doing histology on the inner ear for his entire professional career.
He pointed out that the consensus is that in mammals, cochlear hair cells do not regenerate. This as opposed to birds and fish where they can regenerate. In mammals, vestibular hair cells can also regenerate (Santaolalla et al., 2013).
Where do these 'supernumerary inner hair cells' (sIHCs) the authors of the paper show in their (quite stunning) EM photos come from? I wish to point you to the last lines of the Discussion of your linked paper (Rask-Anderson et al., 2017):

Taken together, it cannot be settled if the sIHC represent renewed or redundant accessory IHCs. Further molecular studies are needed to verify if the regenerative capacity of the human auditory periphery might have been underestimated.

In other words, the extra hair cells may have appeared during development in utero, or perhaps due to regenerative processes later on. Note that the inner ear in mammals is fully developed and doesn't grow anymore in size. The EM photos in the article don't allow for the identification of functionality either. Also note that sIHCs have been identified in the 1800s in other animals and that the beauty of this paper lies more in the fact that it shows that sIHCs exist in humans, rather than showing that IHCs regenerate in man (that would likely not appear in the Upsula journal of medical sciences, but in Nature or the likes). On a side note - the authors of the paper are giants in the field.
Literature
- Rask-Andersen, Ups J Med Sci (2017); 122(1): 1–19
- Santaolalla et al., Neural Regen Res (2013); 8(24): 2284–9


Names of nerves in hands, shins and face

You are looking for the Trigeminal nerve, the largest nerve in the face. Here it is with its branches.

It is both afferent and efferent.

Afferent and efferent components of the facial nerve in the bullfrog (Rana catesbeiana)
Cranial Nerves Illustrated: Figure V-4 General sensory component of the trigeminal nerve, ophthalmic (V1) division.
General sensory afferent (blue-green)


According to the abstract from this paper, the intragastric LD50 of $\Delta^9THC$ (tetrahydrocannabinol) in sesame oil using Fischer rats was 1270 mg/kg. Assuming rats and humans are identical (they're not), for an average-sized adult human weighing 70 kg (~155 lb.), the median lethal dose would be 88.9 grams, or about 3.1 oz.

Keep in mind that's 3.1 oz. of pure THC. That's a lot of weed.


When muscles contract is the process similar to how non-newtonian fluids react?

Calcium ($\ce{Ca^{2+}}$) is a signalling molecule and it acts like a chemical switch that tells other chemicals in the cell to enact the contraction. It's not accurate to think of the cell "filling up" with $\ce{Ca^{2+}}$ since $\ce{Ca^{2+}}$ wouldn't significantly change the volume of the cell alone *. Also, during contraction, the muscle cells contract in on themselves - they don't swell out.

It's also not accurate to think of the cells as hollow. Other chemicals inside the cell (such as actin and myosin) act like machinery that enact the contraction. Instead of thinking of the cell filling up like a balloon, I think it would be better to think of it containing a chemical winch (as in the figure below) whose pulling force causes the contraction. Similarly, instead of thinking of $\ce{Ca^{2+}}$ as a fluid, think of it as a bunch of particles that cause a chemical reaction to turn on this winch when they're allowed into the cell.

Reference: https://www.ncbi.nlm.nih.gov/books/NBK21670/

* During a $\ce{Ca^{2+}}$ spike, intracellular $\ce{Ca^{2+}}$ rises around 10-100x from 100 nM. Assuming $\ce{Ca^{2+}}$ has a 100 pm ionic radius, the volume of the cell ($x$) is only increased by around $10^{-9}x$ to $10^{-8}x$, which is negligible.


Water is split in chloroplasts in the light reaction of photosynthesis. Chlorophyll, acting as a photopigment, captures sunlight and transfers that energy to an electron pair of a water molecule. Under the influence of a water-splitting enzyme (George et al, 1989) it is separated into 2 protons, molecular oxygen and a free electron pair.

Reference
George et al. Science 1989; 243(4892): 789-91


Mass spectrometry versus western blotting for validation

It is a common practice to prove a result using an orthogonal technique. Like RNAseq followed by qRT-PCR etc.

Western blotting is not a robust technique and cross comparisons are difficult because of difference in the avidities/affinities of different antibodies. So comparisons can be made only with one protein-control pair in different conditions.

LC-MS is more sensitive and less biased(IMO). So the general trick is- don't do westerns for all proteins just report the ones that behave well (say that you "chose" these because they are important). I know this is a wrong practice and I should not be advocating it. For your own scientific validation try it with another MS technique; if you used ESI-Quadrupole/ion-Trap etc then try with MALDI-TOF or iTRAQ. Some luddites will continue to cling to westerns.

I think it is better to not test the proteins that have low peptide counts. See what is known as MA plot. This is frequently used for microarrays. Here M denotes fold change and A denotes total expression in both samples. Don't pick proteins that are low in expression in both samples; they might not be meaningful. For example if you have 2 molecules of X and 100 molecules of Y in control condition and 5 molecules of X and 200 molecules of Y in test; then the fold change in X would seem important; however this change may not be relevant and can be a result of stochastic fluctuation/measurement error. If you have many samples you can see if something is stochastic or not but the limitation is the number of samples.

Note: I am not saying that 2→5 molecule increment should be meaningless. But to know if they have a meaning or not you would require more complex models; better avoid them at this moment.


What does a female mosquito need from blood?

According to the Introduction to this paper:

  Attractiveness to biting insects is important in medical contexts, mostly in the dynamics of transmission of pathogens by mosquitoes that cause diseases such as dengue and malaria. Blood feeding is an essential part of the lifecycle for most mosquito species as it provides females with the proteins necessary for egg production.

I imagine that the blood protein is simply a rich source of amino acids. This is supported by the finding that an artificial meal consisting of bovine serum albumin can support egg production in Aedes albopictus.

Update following answer from Greg Thatcher

Clearly there is evidence that iron from a blood meal reaches ovaries and eggs, although the paper doesn't provide direct evidence that this iron is essential. However this made me think more deeply about the paper that I cite above about feeding bovine serum albumin as an blood substitute. Could this have also supplied a significant amount of iron? The artificial meal was BSA dissolved in a phosphate-buffered saline. The authors don't specifically address the problem of iron contamination. The main component of PBS is NaCl. If they used AR-grade NaCl then the iron content will have been very low (0.0002% in one example that I found online). However BSA itself can bind metal cations (see here for example) so the protein may have contributed some iron. The authors do quote the source of the BSA that they used but I haven't been able to access a data sheet that might shed light on the level of iron contamination.

Of course it is entirely possible that blood is an essential source of both protein and iron.


Do animals with crypsis know where they should stay to save their lives?

I think you can break this down into two sub-questions:

Will natural selection select animals whose crypsis and behavior align with each other? The answer here is definitely yes, but with a few caveats:

Crypsis might not be the best strategy in a particular situation: a green lizard crawling on a leaf might be outcompeted with a red-and-blue lizard that is poisonous, for instance.
Either behavior or crypsis might be easier to change over evolutionary time: you might see your green lizard evolving to spend more time in leaves (particularly if it's herbivorous or eats plant-dwelling insects), or you might see it evolving brown pigmentation to hide on the ground.
Natural selection isn't going to be concerned with individual actions but overall behavior. So a lizard might fall off a bush, get spotted on the ground and eaten. But it might dash from bush to bush without getting caught. But if a lizard spends most of its time on leaves, there might be selection towards it being well-camouflaged on leaves.

Does this require a conscious decision on the animal's part? I think the answer here is no, consciousness isn't necessary. Very simple animals show responses to their environment, such as bacteria swimming towards food. Your green lizard might be staying close to leaves that it feeds on, or near the insects it feeds on that itself feed on the leaves, and so stay near the green leaves that camouflage it by accident. Or its brain might be programmed to carry out a complex action to hide it better. Perhaps the most sophisticated examples of this is animals that reconfigure their body to match their surroundings, such as octopuses, cuttlefish (but not, interestingly enough, chameleons!)

This doesn't mean that the animals don't have consciousness or are not deliberately hiding by finding surroundings that match themselves. It just means that that's not necessary to explain why we find green lizards hanging out on leaves.


Is once per day the optimal sleep pattern for all mammals?

So as we know that every mammal needs atleast some amount of sleep or a resting period to perform cognitive functions through out the their day, this however can vary drastically based on the mammal's habits, such as if they are herbivores or carnivores, their place in the food chain (if they are a predator or prey), their habitat, their body size etc.
Starting with humans (to set a point of reference), we ideally need 7-8 hours of sleep in a day. Getting less or more sleep than this ideal can have a lot of different consequences (ranging from feeling tired and foggy to heart conditions and even death). A study performed by a group of researchers to find out the ideal sleep duration in humans showed that just after 14 days the people getting 8 hrs of sleep showed average cognition and a healthy mind, those getting 6 hrs of sleep per day for 14 days showed a similar reaction time to a person with blood alcohol level of 0.1% (which is considered legally drunk in most places), and the group getting 4 hrs of sleep per day for 14 days were tending to fall asleep while performing basic cognitive tasks. This show exactly how important sleep actually is.
Now moving on to some other mammals.
A very commonly discussed example is that of giraffes. Giraffes generally exhibit a cycle of just 2 hrs of sleep per day, and some days they just tend to not sleep at all. A lot of factors contribute to their sleeping habits. Firstly since they are herbivores, and primarily feed on leaves, they need to eat a lot of leaves to get enough energy for their body, having a large body also contributes to this. So, they tend spend about 75% of their day just eating. Other than this since giraffes are prey and a good source of food for lions, they need to stay awake and alert at all times. Sometimes they will take little 10 min long powernaps (this is when they are the most vulnerable, so they don't do it often).
Carnivores however (like lions) sleep a lot more, due to their diets (just like us they feel sleepy after eating) and also since they are minimal risk of being attacked as they are on top of the food chain.
Next lets talk about some sea mammals, they have a hard time trying to snooze because of them being underwater.
Dolphins have very interesting sleep habits as they have to actively come to the surface to breath. Dolphins practice something called "unihemispheric slow-wave sleep", this basically means that they only rest one hemisphere(or side) of their brain at a time(so that they can be awake and asleep at the same time), this is what uni(one) hemispheric(side) means. Slow-wave sleep refers to the deepest phase of sleep, meaning when the one hemisphere is sleeping it is out like a lightbulb. This way dolphins tend to sleep a lot, they have sleep cycle of about 8 hours of sleep a day (resting each hemisphere for 2 hrs at a time). So the dolphins you saw at sea world last year could have been half asleep (literally).
Some birds also practice this uni hemispheric sleep.
I can't think of any animals that sleep "as needed" because activities like sleep and wake are rhythmic and control various hormones and metabolic reactions of the body, this is primarily why we have sleep patterns so that other activities in the body can be done in a habitual manner. This is maintained by our "biological clock", which is the term used to define the natural sleep-wake cycle in animals. The biological clock is regulated by a hormone known as  "melatonin".
So yeah, these were some examples I remembered off the top of my head. I have provided some links to why sleep is important, ideal sleep habits in humans and other mammals and some other stuff for further reading.
Hope this answer helped you understand sleep better.
Sleep: a good investment in health and safety - https://pubmed.ncbi.nlm.nih.gov/19042703/
The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884988/
How Animals Sleep - https://www.sleepfoundation.org/animals-and-sleep#:~:text=Giraffes%20need%20less%20sleep%20than,of%2030%20minutes%20per%20day.
Melatonin: what you need to know - https://www.nccih.nih.gov/health/melatonin-what-you-need-to-know
This is an animated video series explaining sleep in different animals (highly recommend watching this):
Part 1 - https://www.youtube.com/watch?v=HA1EPRbMMQU
Part 2 - https://www.youtube.com/watch?v=EJzUKsJ-uhA
Part 3 - https://www.youtube.com/watch?v=S4uX2KeEifM
Rare Genetic Mutation Lets Some People Function with Less Sleep (this might also interest you) - https://www.scientificamerican.com/article/genetic-mutation-sleep-less/


Is there any kind of antibiotic effective against fungi?

Yes. The antibiotic (general microorganism “targeter”) you’re looking for is an antifungal. There are fewer ways to target fungi as opposed to bacteria, but we can target them nonetheless.

The fungal cell membrane has ergosterol to regulate its permeability whereas the mammalian cell relies on cholesterol. Fungi have cell walls which are not present in mammalian cells and are different in chemical composition to bacterial cell walls. A fungal cell wall is made of chitin whereas, as you mentioned before, a bacterial cell wall is made up of peptidoglycan.

We rely on these differences to target fungi. Some antifungals bind to ergosterol (e.g. Polyenes like Amphotericin-B) whereas other agents inhibit ergosterol synthesis altogether (e.g. Azoles like Triazole). Other antifungal agents target the fungal cell wall by inhibiting the synthesis of chitin (e.g. Echinocandins like Caspofungin).

There are more ways to target fungi, like introducing nucleotide analogues (“look alikes” that don’t work) to disrupt their nucleic acid synthesis (e.g. Fluorocytosine 5-FC). Another method is to disrupt the fungal microtubule’s aggregation during mitosis (e.g. Griseofulvin), thus “arresting” the fungal cells in metaphase.

Recommended Textbooks:

Hugo & Russell’s Pharmaceutical Microbiology 8th edition, Wiley- Blackwell. Edited by S.P. Denyer et al.
ISBN 9781444330632
Essential Microbiology for Pharmacy and Pharmaceutical Science, Wiley- Blackwell. By Geoffrey Hanlon and Norman Hodges
ISBN 978-0-470-66534-3 (pbk.)


What are the molecular mechanisms behind tachyphylaxis (downregulation of receptors in response to an agonist?)

There are many mechanisms of receptor down-regulation, including internalisation and degradation e.g for the epidermal growth factor receptor and uncoupling via post-translational modifcation e.g. for G protein-coupled receptors.

In the case of opioid receptors there is emerging evidence that down-regulation is achieved, at least in part, by post-transcriptional regulation by a microRNA. Presumably this could also accompanied by inactivation of existing receptors, but if the adaptation/desenitisation is long-term then normal receptor turnover may be sufficient.


How do different tissue culture matrices affect background in fluorescent microscopy?

Extracellular matrix (ECM) fluoresces, especially Collagen and Laminin. The maximum is in the DAPI and FITC channels and the fluorescence becomes weaker towards longer wavelengths. However, since the coat on the TC flasks is very thin, I would not expect this to be a problem. The best thing is just to try it. There is also a quite famous document available which might be of help:

Autofluorescence: Causes and Cures


According to Lars Juhl Jensen on a Biostars forum,

  The Proteome Commons Tranche sadly shut down around 2013 due to lack of funding. It is a good example why important bioinformatics infrastructure needs dedicated funding and should not have to operate out of research grants for individual groups.


What bacteria shed harvestable energy from root zone organic matter?

Short answer
It is known that a great variety of soil micro-organisms is able to use solid anodes as electron acceptor for their metabolism, thus creating some electrical current. Geobacter spp., Clostridia and Deltaproteobacteria are among them (1). However, I could not find any extensive list of these microbes. It is likely that a large number of these microbes is not identified yet.
A review on Plant Microbial Fuel Cells was recently published and might interest you (2).
Long answer
Plant Microbial Fuel Cells are a special case of Microbial Fuel Cells
The system presented at your first figure is being developed by the Dutch company named Plant-e and falls within the concept of Plant Microbial Fuel Cells (PMFC).
Simply put, a Microbial Fuel Cell (MFC) is a device in which chemical energy contained in chemical bounds of organic substrates is converted to electrical energy by microbes. Microbes consume the organic substrates while using the anode as the final electron acceptor of their metabolism. Microbes capable of using anodes as electron sinks for their metabolism are called electrogens.
PMFCs are a special case of MFCs, taking advantage of the microbe/plant interactions. Organic substrate is supplied to microbes directly by the plant and you get two benefits: plant biomass and electricity production.
Complex interactions between plant and microbial communities
As you noted in your last sentence, no particular species of plant was cited. Indeed various PMFCs strategies were implemented, based on various species of plants, such as Glyceria maxima, or Oryza sativa (rice) (2). The plant species is not the only key factor for efficient PMFCs: the nature of the organic substrates provided by plants to microbes, the soil's characteristics, the electrodes' characteristics, and the nature of the inoculum are crucial factors too.
Regarding the microbiological aspect, it appears that pure culture (single species) PMFCs are not necessarily the best alternative. Plants provide microbes with a variety of chemical compounds, which may not be all consumed by a single species. Only a well adapted microbial community is likely to be able to take advantage of all these compounds and to include efficient electrogens. The path from plant products to electrical current is more likely to be a complex microbial food web, rather than a single species' metabolism. In practice, most studies seem to rely as soil as the incolum (2).
So, concerning your initial question: we might not have identified yet every soil electrogens. Several are, however, already well known, such as Geobacter sulfurreducens. But, what is important is that most (P)MFCs strategies rely on microbial communities as a whole, in a 'black box' way.

References
(1) Dunaj, S.J. et al. Relationships between Soil Organic Matter, Nutrients, Bacterial Community Structure, And the Performance of Microbial Fuel Cells, Environment Science and Technology, 2012, 46 (3), pp 1914-1922
(2) Nitisovarut, R., Regmi, R., Plant microbial fuel cells: A promising biosystems engineering, Renewable and Sustainable Energy Review, 2017, 76, pp 81-89


How are elements like iron recognized and routed to the right places for use in the body?

A wikipedia source gives you general informations and precise details about the locations and methods of absorption and distribution. Reading the page is well recommended, I will add the quote to save others time:

en.wikipedia.org/wiki/Human_iron_metabolism#Dietary_iron_uptake :

  Like most mineral nutrients, the majority of the iron absorbed from
  digested food or supplements is absorbed in the duodenum by
  enterocytes of the duodenal lining. These cells have special molecules
  that allow them to move iron into the body. To be absorbed, dietary
  iron can be absorbed as part of a protein such as heme protein or iron
  must be in its ferrous Fe2+ form.

  A ferric reductase enzyme on the enterocytes’ brush border, duodenal
  cytochrome B (Dcytb), reduces ferric Fe3+ to Fe2+.[9]

  A protein called divalent metal transporter 1 (DMT1), which can
  transport several divalent metals across the plasma membrane, then
  transports iron across the enterocyte’s cell membrane into the cell.

  These intestinal lining cells can then either store the iron as
  ferritin, which is accomplished by Fe3+ binding to apoferritin (in
  which case the iron will leave the body when the cell dies and is
  sloughed off into feces), or the cell can release it into the body via
  the only known iron exporter in mammals, ferroportin.

  Hephaestin, a ferroxidase that can oxidize Fe2+ to Fe3+ and is found
  mainly in the small intestine, helps ferroportin transfer iron across
  the basolateral end of the intestine cells. In contrast, ferroportin
  is post-translationally repressed by hepcidin, a 25-amino acid peptide
  hormone.

  The body regulates iron levels by regulating each of these steps. For
  instance, enterocytes synthesize more Dcytb, DMT1 and ferroportin in
  response to iron deficiency anemia.[10] Iron absorption from diet is
  enhanced in the presence of vitamin C and diminished by excess
  calcium, zinc, or manganese.


No they are not made of muscles. Glands are modified epithelial tissues. Glands are basically of two types Endocrine and Exocrine glands.

Endocrine gland

It is a gland that lacks a duct system. The secretions are directly
   poured into the bloodstream. They secrete hormones through exocytosis mostly.

Exocrine gland

It is a gland with a duct system. The secretions(sweat, sebum,saliva
   etc) are transported onto a surface of the body (e.g skin or lumen of GI tract) by
   ducts.Exocrine glands may be controlled by muscles at the duct level.

There are three types of exocrine glands based on the process of secretion of chemical substance at a cellular level$-$

Apocrine gland

It is a gland in which the apical portion of the secretory cells are distintegrated to release the chemical. e.g- Apocrine sweat gland

Holocrine gland

It is a gland in which the secretory cells are completely disintegrated to release the chemical.e.g.- Sebaceous gland

Merocrine gland

It is a gland in which the secretory cells remain intact and the chemical is
released through exocytosis.e.g.- salivary gland

Reference:

Wikipedia
ncbi


I cannot say the mechanism, but I can confirm it works, and can say that is generally accepted as working, not as some weird dubious treatment. I had surgery to install a rod in my leg after a broken bone. On the advice of my physical therapist, I purchased "Scar Away" brand silicone oil with roller applicator. Placing a thin layer and massaging with the applicator twice a day for four weeks turned my giant cheloids into small sections of skin which were distinguishable only by their smoothness and lack of hair, not color. He said he used to work for some basketball team and it was common practice to be used in professional basketball.


Can bacteria metabolize fatty acids for fuel?

I found this review about bacterial lipid metabolism. There it says:

  Exogenous long chain fatty acids are utilized by E. coli in two ways. Firstly, they can
  be incorporated into the membrane phospholipids by the acyltransferase system (PlsB
  and PlsC; Section 4). Secondly, they can be used as the sole carbon source for growth,
  and are in fact an important source of energy for E. coli in their normal habitat, the
  intestine [16]. The CoA thioester of the fatty acid is the substrate for both of these
  pathways. Fatty acids greater than 10 carbons in length require the fadL gene product
  to be taken up from the growth medium in sufficient quantities to support growth.

So yes, bacteria can grow on fatty acids alone and they can utilize long fatty acids as an energy source. However the uptake of the long fatty acids requires the protein produced by the fadL gene.


How do plants get their O₂ for respiration during the night?

Not all plants have their stomata closed during the night. A notable exception are Crassulacean acid metabolism(CAM) plants that keep their stomata closed during the day and open it during the night. This is a common evolutionary strategy with Xerophytes.

There are also 2 other types of metabolic pathways namely C3 and C4. As a consequence we get what is called a C3 and C4 plant, which aptly represent the predominant metabolic pathway it employs.

Additionally plant cells, like all life, can produce energy without oxygen by Glycolysis. Furthermore, when stomata is closed, oxygen respiration is restricted, not blocked entirely. Finally it might be important to note that plant metabolism is reduced during the night.

Full disclosure, I am not a botanist. Please let me know if there are any glaring errors.


How to find the amino acid in the DNA protein

Then you just have to read the codon until you reach a stop codon. There are three stop codon UAA, UGA and UAG. So, in your example..

             Start                                                   Stop
5' U A U C | A U G | G C G | U A C | A U G | C C C | G C U | C U G | U A A | G C U C G U A A G U A 3'

Your protein is therefore 7 amino acids long (incuding the starting methionine). The genetic code is

Therefore the 7 amino acids are

Met Ala Tyr Met Pro Ala Leu

In case you are confused about having an AUG codon in the middle of an open reading frame, then you should have a look at the post Effect of a doubling of the start codon in a gene.

Of course, I assumed that the region is indeed transcribed and that the first AUG is indeed the start codon and not just a methionine in the middle of an open reading frame.


What are the predators of Glaucus atlanticus?

Try out using Google Scholar to take a more scientific literature-based approach to your search.

Frick et al. (2009)1 found that about 42% of logerhead sea turtle (Caretta caretta) stomachs contained remnants of G. atlanticus.

  We were able to identify G. atlanticus in the diet of loggerheads because whole or nearly intact specimens were present.

 Loggerhead turtle mouth and throat with sharp papillae. Source NCSU CMAST (Photo by Craig Harms)

Bieri (1966)2 observed G. atlanticus frequently attacking one another and biting off pieces of each other. In one case, one individual ate all but the head and trunk of a smaller specimen.

Citations:

 1, Frick, M.G., Williams, K.L., Bolten, A.B., Bjorndal, K.A. and Martins, H.R., 2009. Foraging ecology of oceanic-stage loggerhead turtles Caretta caretta. Endangered Species Research, 9(2), pp.91-97.

2. Bieri, R., 1966. Feeding preferences and rates of the snail, Ianthina prolongata, the barnacle, Lepas anserifera, the nudibranchs, Glaucus atlanticus and Fiona pinnata, and the food web in the marine neuston.


Simple computational biology project for AP Biology class. Ideas?

You can use BLAST or NCBI resources to do an analysis of something like the duplication of a gene in the HIV virus, for example. If you're looking for a place to start, I would recommend just learning the NCBI database resources.


Bird species ID in the Northern Territory, Australia

That's an Australian White Ibis (Threskiornis moluccus).

It's widespread across much of Australia:

You can find more info on Wikipedia.


The only place that the terms "macro-evolution" or "micro-evolution" are generally used, are in creationist rhetoric. They are not terms used by biologists. This is because there is no need to create distinct categories. In reality there is only "microevolution". Macro-evolution is not a different thing, merely an accumulation of many micro-evolutions.

  what benefits are there to such a broad category as macro-evolution?

None. Which is why such a term has been abandoned.


Why did mammals evolve to have two testes?

EvoDevo is not my field, but I will try to give you some pointers.

Mammals as vertebrates, start out as fertilized oocytes, transform into a rapidly dividing lump of cells with eventual polarity through numerous gradients of numerous chemical messengers, and form a neural tube.
The forming body is ever more segmented through the use of gradients and thresholds (see french flag model) and (dorsoventral) axial symmetry is maintained throughout development, and as such two testes represent the default development.

Therefore, it may be more interesting to ask for singular organs which require more information, and thus maintenance throughout evolution of this information. But when considering the energy requirements, the need for synchronization, the need for a separate blood supply and thus the introduction of additional faults, it is easy to see why we only have one heart.

Wikipedia; author: Zephyris, title: "The first few weeks of embryogenesis in humans", DOR: 25/09/2012

See:

Inversion
Evolutionary developmental biology

I hope this helps as a starting point.


How quickly are plants able to sense changes in light intensity?

The delay for UVR8 photoactivation seems to be in the range of picoseconds depending on the wavelength:

Global analysis in terms of a model of parallel decaying
components indicated four lifetimes of 14.7 ps, 370 ps, 1.9 ns,
and 5.9 ns.

The photodynamics of the Trp ensemble in UVR8 can be summarized as
illustrated in Figure 5B. We observe excited state decay in the
few-hundred- picoseconds to nanoseconds time domain to the triplet
intermediate U460.

<img src="https://i.stack.imgur.com/Sz4zK.png" alt="Tentative photocycle of UVR8
photoactivation as observed in vitro." />
For a better understanding of photoactivation mechanism times, you can read the following article:
Proton-Coupled Electron Transfer Constitutes the Photoactivation Mechanism of the Plant Photoreceptor UVR8
Journal of the American Chemical Society 137(25) · May 2015


What's the highest glucose concentration (in mM) anywhere in the human body (tissue, capillaries, tumor microenvironment, etc.)?

Glucose concentration in the blood is a highly regulated biologic variable. From personal laboratory experience, it is very difficult to raise a healthy, non-diabetic individual's blood glucose over about 6.5-7 mM (i.e. 120-130 mg/dl). My best guess at where the highest glucose concentration might be in the body is within the hepatic portal vein that drains the intestines after a high carbohydrate meal. The glucose concentration is probably highest in the prandial state or, in other words, when carbohydrates (i.e. food) is being digested and absorbed by the gastrointestinal tract. Many simple and/or complex carbohydrates are digested to glucose and absorbed through the gastrointestinal tract. Once absorbed the glucose enters the venous mesenteric circulation and then drains into the hepatic portal circulation. This allows high concentrations of glucose and other compounds like amino acids from dietary nutrients to be "buffered" by the liver.

I don't have hard evidence to demonstrate that this is the highest glucose, but I think it's probably a good guess. It is inherently difficult to measure the blood glucose concentration in the portal vein - mostly because it's so difficult to get to that place anatomically during a meal. The dog is probably the most used animal for these types of metabolic studies, because catheters can be placed in the peripheral venous and arterial circulation, as well as in the portal vein and hepatic veins, to measure nutrient uptake by the intestine and nutrient extraction by the liver.

A number of previous studies by Cherrington and colleagues, who have done some of the most comprehensive work in this field, frequently measure glucose concentration and blood flow rates across the liver. In one such paper that is freely available from the American Journal of Physiology by Abumrad et al (1982) entitled, "Absorption and disposition of a glucose load in the conscious dog" you can see from Figure 1 the average plasma glucose concentration in the portal vein from a group of dogs given an oral glucose load of ~40 grams is somewhere in the 250 mg/dl region (i.e. ~14mM). These were otherwise healthy dogs, and similar to healthy humans I would bet the glucose concentration doesn't rise too much further. As you could imagine though, in a diabetic individual who has high peripheral glucose concentrations to start, the portal vein concentration might be expected to be higher. How much higher is another educated guess - maybe 100-200 mg/dl higher on an extreme end (obviously pathologic).

In a healthy human (i.e. non-diabetic) who undergoes a 75-gram oral glucose tolerance test I can't imagine that the portal glucose would go any higher than 300-400 mg/dl (or, 16.5 to 18 mM). But again - these numbers are just educated guesses. This is probably the highest glucose concentration anywhere in the body. Additionally, in diabetic patients the glucose concentrations would be expected to be slightly higher because circulating glucose may be slightly higher, but probably not by too much (definitely not an order of magnitude).


b+/c+
b/c
b+/c
b/c+

Ada
~0.39
~0.42
~0.08
~0.1

Donald
~0.09
~0.09
~0.4
~0.41

The other chromosome beeing b/c (I assume each one got an heterozygote fly and than they did a testcross)
There are a two possibilities for an heterozygote fly:
(b+/c+, b/c), (b+/c, b/c+)
If there was no genetic linkage we would except 0.25 for each fly group, but we didn't which means that fly groups with a higher probability are showing the original parental chromosomes phenotyping.
Since they didn't get the same results (by far) I assume (there are statistical tests for this) each scientist got a differently genetic fly
Donald got (b+/c+, b/c) since in his experiment the predominant flies are those showing a dominant phenotype and recessive phenotype and Ada got the mixed fly.
With this in mind we can see that the recombination frequency is 0.18 or 18cM
Yes, the recombinant can appear more than the parental (for example, if the parental is lethal or by pure chance) but in this case I belive it is simply a different organization on the chromosomes


How does beta branching stop alpha helices from forming?

The answer to this, as said by @canadianer in comment, is that beta branched amino acids are bulky and can sterically clash with neighbouring atoms, forcing the backbone to adopt torsion angles which don't favour helix formation.

I couldn't find reference for these exact words, but similar one here:

  amino acids such as Valine, Isoleucine, and Threonine all have branching at the beta carbon, this will cause steric clashes in an alpha helix arrangement... valine, threonine, and isoleucine will often destabilize the helix because of branching of the beta carbon. These three amino acid residues are more often found in beta-pleated sheets, where their side chains will lie in a separate plane than the main chain.

Also, for torsion angles, from same source:

  The torsion angle is the measure in degrees in bonds between atoms. Folding of proteins are influenced by the degree of rotation amino bonds can hold. There are two different types of torsion angles existing in polypeptide bonds. Psi, ψ is the angle between the α-carbon and the nitrogen atom of a peptide bond. The other bond is called phi, φ which is the angle between the α-carbon and the carbonyl group.

See this table for details of which amino acid prefers which configuration:

Source


How can potassium rich foods reduce blood pressure?

potassium is really the main guy in charge of everything that happens involving action potentials which in turn govern homeostasis such as blood pressure.

k+ lowers blood pressure due to making it harder to get an action potential going, which in the macro scale causes the heart to pump less.

too much k+ kills the person as it stops the pumping of blood (lethal injections are just lots and lots of k+ along with some pain killing drugs)


Does dormant poison ivy contain urushiol in the above-ground portion of the plant?

Let's tackle your second question first. Yes, leafless poison ivy still contains Urushiol, and still can give you a rash. Here are three sources supporting this statement: a first-aid sales company, a newspaper, and a non-peer reviewed infosheet from a university. Be careful with poison ivy all year.

Your first question has slightly more nuanced implications. To know if there is a time of year where above-ground poison ivy doesn't contain Urushiol, first we have to think about when and where the urushiol is produced in the plant cell, where it is stored, and how it degrades. Some studies have shown that Urushiol and like compounds are present throughout the plant. In this older article, they extract it from both the leaves and the twigs, but more current advances have been able to focus on urushiol in just the stem. I have seen no evidence that it reduces at any time of year, and very little publication on how it is produced biochemically, although people are working and have worked on the topic. I am interested to learn more about this aspect from other answers to this question.

(An aside: you can also pick up a Urushiol rash from some cheap furniture, so this compound can stay poisonous on a wood surface for quite a while. Unfortunately, I'm speaking from first-hand experience, which is backed up by this informative article about Urushiol!)


Distribution of the number of clover leaves

I have found a study [1] of 2017 (http://www.sharetheluck.ch/single-post/How-rare-are-four-leaf-clovers-really) which answers a great part my question, and I'd like to show those results together with some additional evaluation.

They have counted 5.7 million clovers and found the following numbers compared to 3-leaflet clover:

4-leaflet clover    1 in 5,076
5-leaflet clover    1 in 24,390
6-leaflet clover    1 in 312,500

For the 4-leaflet clover they have corrected appreciably the common figure of 1 in 10,000 (see e.g. the comment of Untitpoi here).

A logartihmic plot of these relative frequencies shows interesting features

(i) a fairly regular exponential decay of the frequency in the range n=4,5,6
(ii)    a significant "exception" from this rule is the "normal" clover with n=3

How can these observations be explained?

It would also be interesting to extend the study to n>6, and maybe also to the range of "deficient" clover which posesses only one or two leaflets. The latter are most probably very rare so that the complete log-plot would resemble an inverted letter V.

The question of 2-leaflet clover was raised here [2] https://www.quora.com/What-are-the-chances-of-me-finding-a-two-leafed-clover. But no quantitative answer was given.

References

[1] http://www.sharetheluck.ch/single-post/How-rare-are-four-leaf-clovers-really

[2] https://www.quora.com/What-are-the-chances-of-me-finding-a-two-leafed-clover

[3] https://en.wikipedia.org/wiki/Four-leaf_clover#cite_note-auto-6
A comprehensive reference which I have only partially explored up to now


Prostaglandins A,B,C,D,E,F represent different non-inclusive classes of prostaglandins and all have different chemical structure. Hence (by classification), PgE cannot be subtype of PgF:

PgE have an oxo group at C9, while PgF have hydroxyl group at C9.

Back to Dinoprost, it is PgF2alpha and not PgE2 which is Dinoprostone.


Is it possible to grow any kind of plant soilless (hydroponics)?

Yes it is possible, and as far as I can see, there should not be any plant which would be impossible to grow in a such an environment, just more or less difficult, although this is just my speculation.

I have myself grown tomatoes from only a liquid solution of minerals and nutrients, but you have to change the solution from time to time to prevent bacteria and fungi growing starting to grow in it. The reason why this is not a method used in industrious growing is because it is a lot more expensive than using soil and fertilisers, and more work.


What kind of snake is this? Seen in Peru along the Inca Trail

EDIT: Apparently M. medemi only exists in Colombia, not in Peru. Thus, as I'm not sure about the below ID. Instead of deleting the answer (users with <10k cannot see it), I just turned this into a community wiki, so I don't receive any RP.

By the shape of the head and the structure of the rings, it seems to me that this is a Micrurus.
Of course, the lack of yellow/red rings excludes the most common coral species, like Micrurus peruvianus. So, I'd guess this is a Micrurus medemi.
Here is another picture of it, for comparison:

Source: http://www.planetscott.com/speciesdetail/10840/coral-snake-micrurus-medemi
Some M. medemi specimens have white rings (like in your photo) while some have red rings.
They are venomous, but they are not dangerous: all Micrurus species I'm aware of are not aggressive, and bites are not common. As Wikipedia correctly says:

When confronted by humans, coral snakes will almost always attempt to flee, and bite only as a last resort.

The problem with this ID is that there are reports of M. medemi in Colombia and Ecuador, but not in Peru. I'll keep researching this and update this answer when I find a record (or delete it if I don't).


Is there variability in genetic combination from the same sperm and egg combination

Assuming we know the haplotype of the ovule and the haplotype of the spermatozoid, then the genotype of the future egg is perfectly deterministic. This is true to the extend that none of the following rare events occur:

mitochondria could be inherited from the father as well
mutations in the broad sense (see here for definitions) may occur outside an event of mitosis or meiosis
The egg might pick up random sequence floating in the environment

Of course epigenetics elements might vary but this is another discussion.


You can go to ensembl.org and look up synteny between closely related organisms, like rats and mice.  Below is one example: rat chromsome 1 is made up of all of mouse chromosome 7 and 19, plus parts of 17, 10, and a smidge of 13

https://uswest.ensembl.org/Rattus_norvegicus/Location/Synteny?db=core&r=1%3A126594509-126694509&otherspecies=Mus_musculus


What is this long cylindrical white fruit called?

It appears this is a Kigela (and commonly referred to as a "Sausage tree" in English).

It is - as you suspected - considered inedible and even poisonous in its fresh form (but apparently it can be dried or fermented). It has, as you said, a hard shell which can make this fruit usable as a container after it is hollowed-out.
The wikipedia article on this tree says it grows throughout tropical Africa, but looking at iNaturalist, it has been observed growing all over the world:


Is there a way for a 19th century scientist to prove that the octopus doesn't revive?

Yes. The scientist could cut a small piece of the octopus's tentacle and perform the experiment again. If the same result is observed, no other organs are involved.


Are there gaps in what our ears can hear?

Short answer
No, there are no between-hair cell induced tonotopical gaps in frequency perception.

Background
Young people are able to hear over a frequency range of about 10 octaves, with a frequency resolution of about 0.3% of an octave. So we would have about 2300 resolvable frequencies. This number is dependent on the sound level, as excitation spreads at higher sound levels, but it gives a reasonable starting point to answer your question.

The human cochlea contains on the order of 3,500 inner hair cells. Hence, according to this (highly simplified) calculation, it seems that the number of hair cells is redundant.

In other words, the notion of in-between hair-cell stimulation is stretching the limits of physiological frequency resolution a tad too far.

Reference
- Elliott & Shera, Smart Mater Struct (2012); 21(6):064001

Source
- Cochlea.eu. Cochlea: function


What would cause a single white eyelash?

What Causes Hair to Have Colour and How is Colour Lost?

The colour of hair is due to the presence of melanin, which may be found as eumelanin or pheomelanin. Melanin is produced by melanocytes and is transported to keratinocytes. The hair then grows out from a root at the bottom of the hair follicle. A hair without melanin is a grey hair. The exact specifics of how hairs go grey is quite complex and poorly understood.
The growth and pigmentation of hair grows are both regulated by many factors, including genes such as MC1R and DLX3. This provides some explanation why people of particular ethnicities or families can go grey at different times - their genetic makeup changes how quickly they go grey.
Another factor affecting hair pigmentation is reactive oxygen species (ROS). The generation of ROS (oxidative stress) has been shown to have a role in the greying of hair.. Moreover, ROS are generated by smoking, which could lead to premature greying.
Other factors that have been found to be associated with premature hair greying include UV light, vitamin B12, iron, copper, ferritin, calcium and vitamin D3 (source).

What Would Make an Individual Eyelash go Grey?

As far as I know, the regulation of eyelash growth and pigmentation is very similar to that of hair on the scalp.
Given that the regulation of hair pigmentation is controlled by genetic factors, it could be that there is a change in the function of the genes at that particular hair follicle. This could possibly involve mutations which change signaling pathways, melanin generation, etc. such that melanin is no longer transported into the hair.
There could also be an extrinsic (outside of the body) factor which has locally stopped melanin production. Perhaps at some point, there was an elevated level of ROS or UV light at that particular hair follicle. This could have introduced mutations in the genes, or could have changed how the hair was pigmented.
Alternatively, there could be death of melanocytes in that specific area, which could stop the generation of melanin. There could also be a local change in the levels of the factors associated with greying (e.g. a local vitamin B12 deficiency).

Does Stress Cause Premature Greying?

Surprisingly, despite common knowledge telling us that hair makes us go grey, there is conflicting evidence about this. Stress has been shown to make us go bald earlier but whether it also makes us go grey is not conclusively known. But given that stress has a clear negative impact on health, it's probably best not to be too stressed regardless.


How can they know that they found "all the PERVs"? (porcine endogenous retroviruses)

You are right, they should have written "all currently known PERVs".
Although the structure of ERVs is generally well understood (https://www.ncbi.nlm.nih.gov/pubmed/26104559; https://www.ncbi.nlm.nih.gov/pubmed/26818261) there may be some complex cases that have been missed. Also, the map of the porcine genome is not fully complete yet (nor the human one) so you cannot be sure that there are no ERV-derived sequences hidden in the unsequenced regions.


What is this passage trying to say about Darwin's difficulty in explaining variation?

Remember this is all before the rediscovery of Mendel and the understanding of things like recessive traits and inheritance of discrete rather than blended traits. The problem is that, given an environment in which large beaks are beneficial, over geological time selection will tend to eliminate the small beaks. Then, if the geological environment changes such that small beaks are favored, there are no small-beaked individuals to benefit from the change: they would have been eliminated gradually during the long time when long beaks were preferred. The paradox or difficulty Darwin had was explaining how populations could maintain sufficient variability for selection to act to generate new traits.
This issue is similar to the first: the process of natural selection is all about what happens to existing populations. It explains what happens when you have variation existing in a trait. Natural selection by itself does not explain how mutations could occur to produce those new traits.

Darwin was concerned about both of these issues because at the time he saw them as serious threats to his theory (and specifically, like most good scientists, he worried that these things could mean that he was wrong). It seemed like a weakness of exactly the type he saw in prior works on transmutation of species that he was trying to work beyond. It took a few decades and a lot of scientific progress including the rediscovery of Mendel and the Modern synthesis for these problems to be truly worked out. As for Darwin, the best he could come up with was his somewhat-Lamarckian pangenesis idea, which he defended strongly.


What is this plant with hardened fruits on the beach in Mozambique?

I will take a guess that it is Ficus racemosa which is found in that area. More info. If you have pictures of the rest of the tree that would be helpful.


Why do biologists judge intellect based on brain size?

Your are confusing yourself with your analogy, brains are not like computers. The complexity of the "software" a brain can have is determined by how many cells and therefore connections it can have. In particular flexible (learned) thinking as opposed to instinctual "programs." Brains that are flexible need more cells to allow for more possible connections. Computers are not great analogies for brains they are just the best we have. but to use them a brain is like a solid block of ram, yes a large mass is not necessarily fast but it Can do a a far larger variety of tasks, intelligence is not a measure of speed (flies react way way faster than humans) but generally a measure of how many things you can be computing at the same time. the human brain is basically built to model the entire worlds around us including the brains of other humans, which is many many tasks happening simultaneously. Which is one reason brain size can also be used to predict how social an organism is, (at least in non-kin selected social behavior) social interaction requires modeling many complex things. You also run into the problem with defining intelligence, which is problematic to say the least.

And as another poster has pointed out natural selection will quickly eliminate unused brain mass, (neurons are super expensive to maintain, our brain eats about a third of the calories we consume) so they are strongly optimized for weight, so portions of the brain that are larger should, in general, be doing more to offset the cost, otherwise they will be quickly shrunk. So a portion of the brain that is large must be being used, and must be offsetting the caloric cost, also note many the parts of the brain are fairly basal to the groups being compared like mammals so the so the chances of drastically different fundamental ways of operating are fairly slim.  so if the same portion of the brain is very different in size between two related organisms chances are it is becasue that portion is doing more or less. It is even easier to see with sensory processing portions of the brain, if the olfactory bulb of the brain is huge it has to be due to an increased function in the the sense of smell because it really doesn't do anything else and how the sense functions has not changed. this is backed up by observation the brains of animals with poor senses of smell (like cetaceans) have tiny olfactory bulbs while animals with excellent senses of smell (blood hounds)have huge ones. Intelligence is associated with enlargement and complexity only in specific portions of the brain, not the brain as a whole.

That said brain mass is only a rough estimation.  It more done to control for body mass (which effects brain mass directly) as things like how folded the brain is can drastically alter the complexity without changing the mass much. No one assumes brain size is a prefect predictor for intelligence.


Explanation of the terms "downstream signaling" and "upstream signaling"

It simply means after and before with respect to the flow of information in a given pathway. For example, consider this schematic representation of a pathway:

TF1 ==activates==> gene1 ==produces==> Kinase1 ==phosphorylates==> ProtA

In this schema, Kinase1 is downstream of TF1 and upstream of ProtA. Or, to take a classic example (source):

MEK1/2 is downstream of Raf and upstream of ERK1/2.


Do fruit juices have a diuretic effect & what governs this?

In short: Drinking fruit juice by a healthy person with a normal kidney function do not likely have any significant diuretic effect.

Even if you drink, let's say, 2 liters of 10% fruit juice within 30 minutes, it would likely take about 2 hours for all the juice to be emptied from the stomach into the intestine and absorbed into the blood. Sugar delivered from the intestine will gradually increase blood glucose, but this will be balanced by the glucose taken from the blood by the cells, so, the blood glucose will not likely exceed 11 mmol/L, when glucose can start to move from the blood into the urine and cause diuresis.

I can back up this by the glucose tolerance test in which you drink 1 cup (237 mL) of a drink with ~35% glucose (>3 times as much as in a usual fruit juice). 2 hours after the test, the glucose levels in a healthy person (without diabetes mellitus) will be lower than 7.8 mmol/L, so below the diuretic level (11 mmol/L).


Yes, it's a male.

http://bugmugs.org/wordpress/wp-content/uploads/2012/08/cicada_killer_pair_00052.jpg

Source: http://bugmugs.org/2012/08/cicada-killer-pair/

Update:

Wasps are in general very territorial. Even a paper bag can scare them as they take it as enemy hive. More on this: Do fake wasp nests actually fool wasps?

  Where does this guy go at night?

Wasps are known to be lazy(less active) at night. Probably they go to the nearby mud nest.

  If he's around, I should be able to find some female burrows in the area as well, right?

yes, there are chances of finding a female burrow near by, as they rarely fly away farther than the nest. Otherwise, there main food(cicada) is very heavy for them to carry to the nest.

follow this if you want to find it's borrow: http://www.wikihow.com/Get-Rid-of-Ground-Digger-Wasps-(Cicada-Killers)-from-Your-Lawn


Confused at what is happening with these action potentials

Nice graph. What happens when you reach the top of the potential (when you depolarize the membrane) that you need to go back to a resting potential to be able to stimulized again. The membrane gets "neutralized" and this reaction often over-shoots and goes below the resting potential, which is quite normal. Before reaching the normal resting potential there will be no further activation. The Wikipedia article on the "Action Potential" contains a more complete explanation.


Pyruvate oxidation - where did the hydrogen come from?

The Wikepedia page has a really good diagram of the reactions involved. The Pyruvate Dehydrogenase Complex facilitates the removal of CO2, and the addition of two hydrogen atoms to the overall reaction come from the FADH2/FAD molecule.


Could an exposure to a small amount of viruses result in an easier course of the disease?

I think the answer to your question is actually found in the paragraph surrounding the quoted statement:

  Auch Gunther Hartmann, Professor für Klinische Chemie und Pharmakologie an der Universität Bonn, berichtete, nach ersten vorsichtigen Einschätzungen sei davon auszugehen, dass der Schweregrad der Erkrankung über Hygienemaßnahmen reduziert werden könnte. "Die Zahl der Erreger hat bei Erstinfektionen Einfluss auf den Schweregrad der Erkrankung."

Approximate translation:

  Gunther Hartmann, Professor of Clinical Chemistry and Pharmacology at the University of Bonn, also reported that, after initial careful assessments, it could be assumed that the severity of the disease could be reduced via hygiene measures. "The number of pathogens influences the severity of the disease in initial infections."

Notice that the language is not absolute but rather asumptive: "initial careful assessments," "It could be assumed," "could be reduced."  It's tentative language and suggests that research is ongoing.  Furthermore, if you search for that quote, you'll find that this is not published in peer-reviewed journals; it's simply a preliminary observation to encourage the public to limit intake of pathogens.

We already know that in some other cases the viral load affects the severity of symptoms. But we don't actually know that that's the case with COVID-19.  In fact, initial reports from Italy suggest that there is no statistical difference between viral loads between symptomatic and assymptomatic cases of COVID-19. So Chris's short answer is absolutely right; we don't know.  For all practical purposes, it's just as well to assume that it's the case, as it will lead to more hygeinic practices, but further research will be required to demonstrate that it is actually the case.


books for beginners in research in mathematical biology

Probably the best contemporary book taking a broad view of mathematical biology modeling is Otto and Day's 2007 book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution published by Princeton University Press.

There are also a number of books that focus on more specific areas e.g. mathematical population genetics, ecological modeling, infectious disease epidemiology, etc. But without knowing which areas of modeling interest you it is difficult to recommend at this level.


There seems to be quite an amount of resources to help OP.

Addgene has a page on topic with list and description of common promoters usable in variety of organisms: Plasmids 101: The Promoter Region

Experimental biophysics textbook mentions some useful promoters as well, or this review.

Surprisingly, there has been some quantitative analysis of promoter strength: Systematic Comparison of Constitutive Promoters and the Doxycycline-Inducible Promoter, as well as effort toward stronger synthetic (version of CMV) Synthetic design of strong promoters

My conclusion is that either viral, or CAG (based on chicken actin) promoters might be useful candidates. But one cannot expect ubiquitous and even expression in various tissues/cells types without fine-tuning expression cassette.


tandem repeat sequence; causes of contraction and/or expansion question

Gene-duplication would not result in contraction (only expansion). Endoduplication would affect all the genes in the chromosome. Error prone repair would cause small-indels but not expansion of the repeats. Inversion will certainly not do anything to the sequence except changing its orientation.

During unequal crossover, the chromosomes can align imperfectly because of multiple alignment sites in the repeat region, thereby leading to unequal crossover products.  Crossing over however essentially happens because of homologous recombination. Crossover is a "phenomenon" and not a "mechanism" in a true sense.

  Mechanism of crossover

  Reproduced from: Bugreev, Dmitry V., et al. "The resistance of DMC1 D-loops to dissociation may account for the DMC1 requirement in meiosis." Nature structural & molecular biology 18.1 (2011): 56-60.

Another thing to note is that homologous recombination in the absence of crossover can lead to expansion of repeats but not contraction (see below).


Book recommendation: protocols and recipes handbook for molecular biology / biochemistry

I know you are asking for books, but for up-to-date basic overview of how some methods work - I would try websites or YouTube instead of textbooks...
One good website is BiteSizeBio. They have their own section for 'how to articles' and educational webinars. Otherwise I would also try YouTube. If you search in YouTube for basic techniques like 'how does the ELISA method work?' or 'principles behind SDS-PAGE' then you will find a lot of instructional movies. There is also the 'the protein man's blog' for purification of proteins, some analysis but also some DNA things.


What is the energy produced by the mitochondria?

The use of the energy in ATP is quite complex. Since my college days our knowledge of how ATP is used has broadened considerably.

Let's look first at the role of ATP in the sodium-potassium pump. This pump uses roughly 20% of the ATP your body produces, even more if you are a couch potato. ATP powers this process by attaching its terminal phosphate group to the pump. The phosphate group is highly charged. Its attachment pulls and tugs on some regions of the pump and repels other regions due to the fact that many of the amino acids comprising the pump are polar or charged. These electrical, magnetic-like, interactions change the shape of the pump. This causes sodium ions to be pumped outside the cell even though they are more plentiful there. When the phosphate is released, the pump returns to its original shape bringing in potassium ions and reloading sodium. It is this pumping action that, among other things, provides the energy for messages in nerve and muscle cells (action potentials).

Probably the important energy use of ATP is this. Many of the reactions your body needs are uphill battles. That is, there is more energy in the substances we wish to produce (products) than in the substances which we must use for raw materials (reactants). So, the ATP attaches its phosphate to the reactant. This raises the energy in the reactant making it now have more energy (more unstable) than the product we wish to produce. The reaction now becomes "downhill" and can proceed naturally ("spontaneously") without holding a bunsen burner under your bottom. This concept is termed "coupled reactions" where we take the "downhill" breaking down of ATP and use it to power the "uphill" production of a requires substance.

There are two principal reasons a molecule becomes more energetic when a phosphate is attached. It is now more complex. Complexity increases instability, a consequence of the laws of thermodynamics. Another reason is that the highly charged phosphate creates stress in the molecule due to electrical interactions with other parts of the molecule.

Here's an image (mine) to show the concept of coupled reactions:


How much light can pass through the human eyelid?

Short answer
About 0.79% of the light gets through on average, but there is variability across wavelengths and individuals. (variability between individuals seems to be correlated with density of macromolecules in the eyelid).
Long answer:
This is called "eyelid spectral transmittance".
Lucky for you, Bierman et al (2011) sought to determine the answer to this question.
Using a custom LED wand that actually emitted light under the eyelid for a sensor on the outside to read, they found quite a bit of variability both across wavelengths as well as across 27 test subjects.
They report their findings in terms of optical density, which is explained as follows:

A measure of the transmittance through an optical medium. Optical density equals the log to the base 10 of the reciprocal of the transmittance.... In spectroscopy, optical density is the measure of absorbance, and is defined as the ratio of the intensity of light falling upon a material and the intensity transmitted. Abbreviation OD.

We can use the equation  A = -log10(1/T) to convert their findings of OD to transmittance and then multiply by 100 to get a percentage of light that can pass through.

Their result of an OD of 2.1 ± 0.3 SD = a transmittance of 0.79%

They do note that  eyelid thickness, and/or the density of macromolecules in the eyelid account for most of the variation in transmittance between subjects.

 Bierman, A., Figueiro, M.G. and Rea, M.S., 2011. Measuring and predicting eyelid spectral transmittance. Journal of biomedical optics, 16(6), p.067011.


Major groups of photosynthetic prokaryotes

To answer your question, yes they are all in a different genus, but that’s really specific.  If you are wondering about their fundamental differences, they fall into a few different groups.

Green sulfur bacteria usually falls into the phylum Chlorobi

Green non-sulfur bacteria falls into the phylum Chloroflexi (Part of the terrabacteria superphylum)

Cyanobacteria is a phylum in itself but also falls into the terrabacteria superphylum.

Both, Purple sulfur/non-sulfur bacteria are all proteobacteria.

Now, pay attention here, as linking these could be somewhat confusing sometimes.  But now we can link together their relationships.

Green sulfur bacteria (Chlorobi) falls into the FCB superphylum, meaning that it is a gracilicute.

Purple sulfur/non-sulfur bacteria (Proteobacteria) are also gracilicutes.

Green non-sulfur bacteria (Chloroflexi) is part of the terrabacteria superphylum.  Terrabacteria are not gracilicutes.

Cyanobacteria is also in the terrabacteria superphylum. (Again, not a gracilicute.)

Now that we know this, we can reasonably assume that both purple sulfur/non-sulfur bacteria are related to green sulfur bacteria, as they are both gracilicutes.  Also, we can conclude that the non-gracilicute green non-sulfur bacteria and Cyanobacteria are more closely related to each other than they are to the latter mentioned bacteria.

Here’s another cool fact, some Deinococcus-Thermus bacteria (members of the terrabacteria superphylum along with Cyanobacteria and Chloroflexi) have been found to carry the bacteriophytochrome photoreceptor (BphP) which absorbs red light.  Interestingly, Deinococcus-Thermus are non-photosynthetic, but these photoreceptors are found in photosynthetic Chloroflexi as well. This indicates that the deinococcus bacteria likely diverged from chloroflexi at some point but still retained the BphP.

Hope this helped!


Looks like Nerium oleander based on the leaves and the seeds/pod.  If not that species, certainly in the genus.  This is a common landscape plant in arid environments, and native to your area according to Wikipedia.  It contains extremely toxic substances that affect the heart, called cardiac glycosides.  Consuming these substances, which are found in the white latex, causes the heart to beat itself to death.


How to induce a steady increase in cyctoplasmic [Ca2+] in HEK293T cells? And is there any simple marker/method to confirm it?

As far as I know, microscopy (be it with dyes like fluor or with genome-encoded calcium indicators) is really your only good bet, especially for getting quantitative sensitivity, which I think is what you're looking for. Changes in cytosolic calcium are incredibly dynamic both in time and space, which is something to consider when asking how calcium affects your two proteins.

I do know of an example where investigators transferred cells to buffers with different Ca2+ concentrations and permeablized them with a mild detergent to raise calcium levels (Borges-Pereira et al 2015). I'm not sure if that would work for your system, but it's worth taking a look, as I think it raises the levels pretty gently and steadily, and you have a better idea of what your intracellular concentration is going to be without directly visualizing it. Considering you won't be able to tell the Ca2+ concentration at any given time without microscopy, things like SOCE and intracellular chelation rates might be important, so you'll want to watch out for when after treatment you start your assay, perhaps trying a few different time points

Hope that was of some help!


Do marine deep sea life forms exhibit circadian rhythms? If so, what entrains them?

A research paper that recently came out suggests that deep-sea life does have a circadian rhythm, but it is regulated much differently than it is by us surface dwellers. We see light, we eat and digest, and the suprachiasmatic nucleus in the brain (our "biological" clock) keeps track of it and eventually establishes a rhythm of the circadian variety.

Most living things at the surface have some sort of circadian rhythm - the mechanisms vary, but they are present and can be readily observed.

In the deep sea, the mechanisms are quite different since they can't see any light, but the rhythm is still established. When these animals (squid in the research) eat a certain type of bacteria containing a light organ, the presence of certain proteins within that organ actually trigger a change in the gene transcription responsible for encoding the protein controlling the circadian rhythm. Thus, when the squid eats, it ultimately determines what the rhythm will be. The entrainment itself actually happens by means of the light organs consumed in the bacteria.

As far as where the bacteria ultimately get there bioluminescence, there is still research to be done, although I would presume there is a mixture of downward bacterial migration and chemical generation contributing to this.

Link to the article: http://mbio.asm.org/content/4/2/e00167-13


The slight curve allows bone to absorb shocks better.

This curve allows the bone to act like a spring and flex a little bit. One issue as bone get older is that they become harder and, therefore, more brittle which leads to the elderly breaking bones for a fall that younger individuals just get a bruise. Young children often get stick or "splitting" breaks where the bone does not break but separates as the bone is still soft.

The ends tend to be thicker as that is where the joints are and there are forces that need to be absorbed.

Of course, if the load applied to the bone is just too much or it is a sharp shock then bones will break, but really the skeleton is nature's design for a suspension system to allow us to do what we need to do walk, run, stand, etc

This set of slides makes good reading, with things like "less ductile", "elastic behaviour" and "strength in compression" worth looking for:

Mechanics of bones by Phillipe GILLET

A quick search gave many results but of these two shown the first seems very interesting from an engineer's perspective:

shock absorbing "goo"
shock absorbtion


Why does the HPV vaccine not work on already infected people?

This is an excellent question, and it is actually being studied -- but for a different reason than your question suggests. HPV is a bit unique because there is some data showing that infected individuals can become "reinfected" with the same virus type, causing reactivation of the dormant/latent virus that they are already infected with. So the question in this case is whether administering an HPV vaccine to an already infected individual can help prevent (or minimize) reactivation of the latent virus.

Here's a journal article explaining some of this research. Please note that it is not standard medical practice to give HPV vaccine to already infected individuals. This work is still in the research phase, and is aimed at minimizing viral reinfection and reactivation:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006803/

Simply put, a vaccine only works to prevent infection with a specific virus. It is rarely effective in treating a virus once a person has become infected. The reason for this has to do with how the immune system responds to its first encounter and subsequent encounters with a particular virus:

When the body encounters a specific virus for the first time, the immune system mounts a "primary" immune response specific to that virus. A primary immune response triggers the body to produce virus-specific immune cells that can generate antibodies against that virus. The body continues to make these immune cells in small quantities even after the virus is eliminated.

If the same virus is encountered again later, these cells will proliferate and immediately start producing antibodies against the virus. Thus, the body can mount a much faster and stronger "secondary" immune response. This prevents the viral load from reaching levels that produce physical symptoms, so the person does not become sick (or at most they may have milder symptoms), and the immune system is to able eliminate the virus more quickly.

The purpose of a vaccine is to trigger a primary immune response. With a vaccine, the body is exposed to a weakened form of the virus, and a primary immune response is triggered without the individual becoming sick. When the individual encounters the real virus, the body immediately mounts a secondary immune response, which fights off the virus much more efficiently and quickly, and the person typically has no physical symptoms.

Here's a more in-depth explanation on the difference between a "primary" and "secondary" immune response. Most cell biology textbooks (and all immunology textbooks) will have an explanation of this as well. This is an important concept in understanding how vaccines work:
http://www.microbiologynotes.com/differences-between-primary-and-secondary-immune-response/

If a non-vaccinated person is infected with a virus, administering a vaccine generally has no effect. At that point the body is already mounting a primary immune response, so a vaccine would serve no purpose. Because a primary immune response is slower than a secondary response, when a non-vaccinated person gets infected the viral load is able to increase more rapidly than it would in a vaccinated individual, resulting in the physical symptoms typical for that particular virus.

What makes "chronic" viruses such as HPV and Herpes virus (including chicken pox) harder to eliminate completely is that these viruses enter a dormant/latent (lysogenic) phase. At that point they become "invisible" to the immune system. Even if the person is not visibly sick, they are still infected with the virus. If/when the active (lytic) phase is triggered, the viral load increases rapidly -- more rapidly than if it were a new viral infection. The body still mounts a secondary immune response, but typically this will not completely eradicate the virus. As long as any amount of the virus is in the lysogenic phase, it remains "invisible" to the immune system.

With some viruses (e.g., chicken pox virus, which causes shingles) if a vaccine is administered during the latent phase, this can help somewhat with making symptoms milder if/when the lytic stage is ever triggered. But this doesn't work for all viruses.

If a targeted antiviral medication is available (e.g., Tamiflu for influenza; Harvoni for Hepatitis C) this can slow down the proliferation of the virus, allowing the immune system to "catch up" and eliminate the virus. Antiviral medications aren't vaccines. They are designed to directly target the virus and interfere with a biochemical activity that the virus needs in order to proliferate.

Currently there is no antiviral medication available for HPV, although a few drugs are being researched. One drug in particular (ranpirnase) looks promising, but it is still in early clinical trials.


Effect of histidine on the binding affinity of HisP

Still if you change your question as (If histidine is abundant, HisP's job is to stop the histidine pathway as a "repressor." If HisP binds less tightly to promotors, the pathway should not produce as much histidine.)
Then it should be under another assumption that what is the effect of HisP binding promoter of enzyme's gene. Is it suppressing the transcription or amplifying the transcription.
If it suppresses transcription then answer is more tightly, if it amplifies the transcription then answer is less tightly. I suggest you put this clearly in your answer, as the question is not quest accurate.

I guess your answer might be wrong.
The question should be under another assumption that how does this protein HisP regulate histidine biosynthesis. positiver or negative feedback regulation.
Generally, amino acids synthesis is regulated by negative feedback loops so that cells could control the amount of amino acids they want. In this case, the answer should be more tightly. As it functions as a repressor then it should bind promoter more tightly so that to repress the transcription more which then generate less histidine synthesis enzyme. (I believe this is what your teacher want you to answer)
In the other case, biosystems sometimes have the positive feedback regulation so that they can amplify the sensitivity to the environment noise or generate bistability (phenotypic switching). In that case, the protein bind promoter less tightly in order to generate more histidine.


Did early 20th century researchers state why they used E. coli as a model organism?

Historical Fallacies implicit in the Question

  “…why a researcher chose to use E. coli as a model organism.”

Researchers did not work with E. coli because they regarded it as a “model organism”. They worked with it because they were bacteriologists and it was a convenient bacterium to use. As Joshua Lederberg wrote in Microbiology Today (2004):

  From the beginning, although pathogenic strains were also found, E. coli was used as a representative, harmless bacterium that could be safely and easily cultivated even on synthetic media. On rich media, it will grow with a
  doubling time of 20 minutes; hence readily visible colonies can be seen overnight when it is plated on agar. Specialized media, like MacConkey’s agar,were developed for the selective isolation and identification of E. coli, as this was used as a global indicator for the pollution of water supplies. Hence, during the first half of the twentieth century E. coli was well known to bacteriologists. However, it was rarely, if ever, mentioned in general biology texts, as bacteria were generally regarded as pre-cellular in complexity and devoid of the nuclei and other genetic apparatus of ‘real’ organisms.

Indeed the term ‘model organism’ was not used in this sense until about 1970, as this Google ngram shows.

  “I imagine that prior to the widespread use of E. coli, scientists would have had to argue why they chose to use it to investigate biological phenomena not limited to this bacterium alone.”

You imagine wrongly. They were not sitting down and saying “we want to study this biological phenomenon, what bacteria shall we choose?” and certainly not having to justify themselves on publication. In general they published in specialized bacteriological journals where audience and referees would know why they were using E. coli or whatever. Even when Tatum and Lederberg (see below) published a letter on bacterial recombination in the general science journal, Nature, in 1946 they did not waste space on species justification:

No. You are imposing modern attitudes — governed by the contemporary state of science and its funding — upon the science of a completely different era. That is not the way to approach history.

Why did E. coli become the most studied bacterium?

It would seem that the discovery of bacterial recombination in E. coli by Lederberg and Tatum (for which they shared the 1958 Nobel Prize for Physiology or Medicine with George Beadle) was one of the key factors leading to the expansion in the use of E. coli (see Microbiology Today article previously cited). This phenomenon was originally suggested by studies on the transformation pneumococcal bacteria, but its demonstration in the bacterial workhorse, E. coli, opened the doors to the use of a wide range of genetic techniques that could be used for biochemical, as well as molecular biological, studies.


Inhalation and exhalation happen sequentially as Herman stated in the comments.

Yes, your general understanding of inhalation is correct. After the air gets into the lungs, the oxygen is diffused into the capillaries covering the alveoli. The now oxygenated blood travels back to the heart to be circulated throughout the body. As this blood enters capillaries in other regions in the body, the oxygen diffuses out of them and into the surrounding cells. Carbon dioxide (CO2) produced by the cells as a waste product then diffuses into the blood vessels. The CO2-rich blood is then circulated back to the heart to be pumped back to the lungs. This blood flows into the capillaries surrounding the alveoli, and diffuses out. The exchange of carbon dioxide and oxygen occurs simultaneously. So, as oxygen is diffused from the lungs into the bloodstream, CO2 in the bloodstream is diffused out into the lungs.

Here are diagrams to depict what is described above.


Do bigger animals have more testosterone?

It is not that easy. Off the top of my hat I can try to pinpoint a few fallacies in your theory:

Scaling of the body happens in three dimensions and thus to a power law. As such allometric equations have to be applied when dealing with the total amount of substance in the body. Different species have different correlation factors of body mass to total substance amounts.
Angiogenesis (the formation of blood vessels) is affected by Allometry (the relationship of body size to the 'biology')
Diffusion factors are similar in closely related species. This means in order for messenger molecules with a short acting range/half-life (e.g. nitric oxide), the total amount in the animal may indeed be likely higher and the messenger in question may be produced on-site (e.g. endothelium). Testosterone as the name indicates, is however produced in the testes and released in the blood stream.
The sensitivity and regulation of the receptors themselves (which react to a substance) can be different in different species. It may also be weakly responsive to begin with at the genetic and ultimately the folded protein level. A good example of that is the melanocortin receptor MC1R in a gross section of the white human population. Even if you were to produce the same level of melanotonin, the melanocytes wouldn't respond to the same degree as in Humans with darker skin.
Messenger molecules can be re-purposed and take over or be given additional roles and functions over evolutionary-time. Again, Melatonin may serve here as an example.
After all a given messenger is already evolutionary tested, especially in regard to cross-talk, Haptens, and other adverse molecular interactions in the animal species and comes with the full set of molecular machinery adapted to it, - a "luxury" a new messenger doesn't have. As such pressure usually exists to re-use given messengers.

  Like, in animals, does testosterone correlate with size, possibly
  explaining why a lion is heaps more slender, muscular, fit, agile,
  aggressive, and vicious than a typical human?

I doubt you will find typical humans or typical human populations from a biological perspective. Your view may be skewed by economic factors.

  Basically, does the bigger size and aggression in wild animals
  correlate to their higher testosterone, such as larger size equal to
  larger testosterone in comparison to other smalelr or less aggressive
  animals, or is it different?

To a large degree the behavior is determined by the niche the animal is in. As to which concerted molecular messengers make the "evolutionary cut", by best influencing an animals behavior in its given "time-domain" is another question. As the question is complex much is still researched.

Take this counter-example: A mouse and an elephant have very different masses resulting in different inertial forces. Fleeing from an enemy will take different strategies in regard to the central nervous system as well as the body, and demand different levels of messenger molecules at different places, at different times for both animals. Yet the substances in question will likely be similar.


Common Ancestry of ETCs and ATP Synthase complexes

Rickettsia and Cyanobacteria are not part of a small clade that share these features.  ATP synthases are present across all domains of life, and they are all homologous, i.e. derived from a common ancestor.  The means its fairly likely that the last universal common ancestor had some form of ATP synthase.

ETCs and ATP synthases are part of the chemiosmotic theory put forward by Mitchell.  Whats beautiful about this mechanism is that you just need a single ATP synthase to make your energy, and it can be used regardless of your metabolism, be it a Cyano or a Rickettsia.  All you need to do is somehow couple your metabolism to a proton motive force across your membrane, and then you just let the protons fall back down their electrochemical gradient, powering the formation of ATP.

Organisms from all corners of the tree of life use this strategy, so this is not some special common feature linking the organisms that ultimately became eukaryotic organelles.  Its worth noting that there are alternatives to ETCs and proton motive force-based ATPases, you can make ATP by substrate-level phosphorylation like in fermentation metabolisms.


Determining and Differentiating specific ATPases

First of all, I think you need to research the subunit structures of the various ATPase classes in the list because I am pretty sure that several of them are not as complex as this.

Although this superficially looks like the F-ATPase responsible for synthesising ATP by using the proton gradient generated by the electron chain, there is a clue in that diagram that this may actually be a V-ATPase. The V-ATPases use ATP hydrolysis to move protons from the cytoplasm into the lumen of acidic organelles like lysosomes. The diagram in the question depicts a process like that (ATP is being hydrolysed). Now, you can drive the F ATPase in reverse to achieve this situation, so that isn't definitive.

The labelling of the two compartments is also consistent with the idea that it is a V-ATPase since 'lumen' isn't a word that is usually used in the context of the mitochondrion (it would normally be 'matrix').

So I would suggest that you find out if the subunit labelling is like that used in F-ATPase or V-ATPase (or both). A Google image search will help you to find cartoons of ATPases.

My guess, before doing the suggested research, is that this is a V-ATPAse.


Okay, I found the last part of your question the most interesting and can't give a full answer to that, but I just noticed I can answer the rest so here goes.

How it works (the simple version)
It works on the principles of buoyancy. The eggs and oocysts are less dense (lighter) than the fecal flotation solution and, consequently, they float on the very surface of it. The feces themselves are more dense (heavier) than the fecal float solution and, as a result, they sink to the bottom of the solution, out of the way. Commonly used flotation solutions include sodium nitrate, Sheather's sugar solution, zinc sulfate solution, sodium chloride solution and potassium iodide solution.

The eggs of some important parasites (for example. Schistosoma species and Fasciola hepatica) are more readily diagnosed by fecal sedimentation (sediment) tests because their eggs tend to sink in flotation media.

What makes it so important?
Some parasite eggs float and some don't. Faecal flotation is a simple, rapid and helpful diagnostic that narrows down the agent causing the clinical signs in the animal.

How it's done
Use a "Fecalyser", a commonly used test kit for faecal floats. The best stool samples to get are those that are fresh - straight out of the animal within the last 30 minutes where possible. Detailed walkthrough of the protocol here and video tutorial here.

Why is there a difference in the buoyancy of fertilised versus unfertilised eggs?
No idea, sorry.  Similar effects are seen in some insect eggs - Stomoxys eggs which sink mostly hatch, while floaters don't hatch. The fact that Anopheles eggs have floats and Culex lay egg rafts implies to me that their viable eggs would otherwise tend to sink too (this could be to do with oxygenation levels being higher at the surface, but I'm speculating here). During embryonation, a serosal cuticle forms which makes the eggs highly desiccation-resistant; non-viable eggs dry out. However, according to some sources online it sounds like for parasite eggs it's the unfertilised eggs which sink, not the fertilised ones.