text:
Photosynthesis and thermosynthesis(?) in plants/organism
A while back I thought to myself: if plants could absorb the entire(or most of) light spectrum as opposed to a narrow range, would it be better/absorb more energy/etc. Recently i read that was not the case because any higher on the spectrum and it could knock electrons loose(or something like that) and any lower and it would generate heat instead. Also the article said that plants focus on specific wavelengths for photosynthesis, hence the colors.
If heat is the main issue, then is it possible to turn the heat energy into usable chemical energy? Potentially allowing plants to absorb a much larger range on the light spectrum? And if the plant could absorb heat as well, would it be cool/cold to the touch?

Theoretically it should be possible for an organism to use hat to produce a chemical that it can then use to make useable energy however at present we know of none that do this. If it is possible though it would allow for life in the warm, dark oceans of Europa and if life is not there already it would make it pretty easy to introduce life permanently to a planet like the moon Europa. However in deep sea vents types of anaerobic respiration are most effective and on the surface light is and so if any organisms ever did use thermosynthesis on earth they were probably outcompete do by other forms of energy production and forced to extinction.

Welcome to Bio. Could you add sources to your answer?


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Can you identify this bee?
Found on the ground on dried cottonwood leaves in southern Utah.

It looks like a species of Megachilidae family of bees, solitary and leaf eaters, covered in pollens.
It could be from Genus Megachile.
All its identifying features are hidden though:

T1 segments have 2 “sides”, one that faces forward or faces the thorax and one that faces the top.$^1$
In Megachile, the “corner” where the forward side and the top side meet is severe. It creates a flat or concave appearance like a circular shelf.$^2$

This genus it comparable to Lithurgopsis which

has a more gradual transition to the "sides" of T1.$^3$

(Source: bugnet)

@MikePasichnyk I didn't ID this correctly. Your bee shouldn't be a leaf eater, as the  pollen-carrying structures of this family are restricted to the ventral surface of abdomen. So it is anything other than this family. I'd like to remove this answer which is possible only if you uncheck it.

Tyto is correct, it's not a megachilid. It looks like it's probably in the genus Andrena to me, you can see deep, hairy fovea at the top of the head.

source: Stack Exchange

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

sort: votes


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How do plants store energy by potassium battery?
Plants have a so-called potassium battery system for energy storage/conversation. Wikipedia only has a reference to a technical article. Can someone explain it in a layman's language (or refer to a non-technical article)?

Oof, I'm not much of a fan of that Wikipedia article's segue to a "biological potassium battery" since the mechanism and purpose is totally different. The cited article is fine but the summary in Wikipedia is taking a statement in the article way too literally.

@BryanKrause I guess that wikipedia page is not properly curated. It also says that Prussian Blue is a potassium compound (it is Fe₄[Fe(CN)₆]₃)

@WYSIWYG Good catch, I hadn't really looked at the quality of the rest of the page. Yet another reminder to be a bit careful with Wikipedia...

I'll give it a layman's attempt in sort of an "ELI5" approach. I hope the analogy isn't too simplistic, and please don't take it too literally.
How do plants use K+?
Plants control K+ concentrations and do work within the plant by pumping K+ between different compartments. Because water tends to follow solute concentrations (osmosis), plants can do things like suck in water simply by moving potassium around.
(note: animal cells do something similar: this is how your nervous system, kidneys, digestive tract, and other cells/organs perform their functions, but using different ions or combinations of ions)
Analogy to some human activities
Moving all this K+ around takes a lot of energy. Creating a concentration gradient is a lot like pumping water uphill: you put some energy in, but you are storing that energy as potential energy for the water flowing back downhill, or the ions flowing back against their concentration gradient (or water flowing the other way). But normally, plants use this as a way to spend energy to do useful things, rather than a way to store it. It's like they are pumping the water up the hill and then floating useful ores or lumber on a boat as it flows back down the hill.
What is actually happening that Wikipedia describes as a plant "K+ battery"
The article cited on Wikipedia, though, Gajdanowicz et al 2011, shows that sometimes plants take advantage of the mobility of potassium ions to assist the H+ ATPase that is another form of energy storage. Plants use H+ (proton) concentration gradients similarly to how they use K+ concentration gradients, but they are used to power different processes in the plant. Sort of like two different types of batteries.
Return to the analogy, and why this is useful to the plant
Normally both H+ gradients and K+ gradients are powered by ATP, which is indirectly produced via photosynthesis: think of it like the plant's coal-fired power plant. Converting K+ concentration gradients to H+ concentration gradients would be like using the water you pumped up the hill to power a hydroelectric plant that is charging a car battery. The benefit for the plant is that, because K+ can be easily moved around, the plant is able to power those hydroelectric plants anywhere around the hill, and that can be advantageous if a particular part of the plant is low on other sources of energy.

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Do cells in healing ligaments or tendons have deformation processes? If so, what are they?
I am trying to better understand how non-muscle tissue in the muscuoloskeletal system heals. Specifically, I am interested in how ligaments or tendons heal once torn.
I read the following text:

If the muscle pulls the damaged tendon and then releases it then we have a deformation cycle that the cells are able to detect. They also then receive the information they require regarding orientation. This is why the elasticity of the early callus is important; the tissue must be able to be pulled out and then return to its original shape in order to receive information about orientation.

Source:
http://www.peraspenberg.com/texts/how-do-tendons-and-ligaments-heal/
I don't understand what they mean by "deformation cycle" and how cells detect it.
Is there a name for this cycle? If so, how do the cells detect tissue deformation?
Also, if there is any literature that specializes in the tissue of ligaments or tendons, recommendations would be appreciated. I have plenty on muscle tissue and some on bones, but not ligament or tendon tissue regeneration.

Are you asking about tendons or ligaments, or both? Your quote only discusses tendons. Your title only mentions ligament. And in the question's details you asked about "the tissue of ligaments and tendon formations"

You are correct, it was ambiguous. I updated it. Is it clearer?

Thanks, that's clearer. Why did you reject my edit? it was pretty much the same as yours and in addition to it was fixing tags, typos, and dead link.

@FranckDernoncourt Because I didn't read it clearly enough and did a bad job. If there was a way to resurrect your edit and do it again, I would approve it. At the time, I read the title and the first few lines, and it seemed to be changing the content. Then you called my attention to it again and I realized it was probably an experienced person editing it or they wouldn't care. When I reread it carefully, I realized you were right. I get a lot of edits that just make small changes, so I might have been trigger happy on reject.

@FranckDernoncourt Sorry about that :/

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Why arent mosquitoes found near neem trees?
I read an article yesterday that wherever neem trees or spices are cultivated mosquitoes are not seen there. So why arent  mosquitoes seen near these places (neem trees , spices, etc).
What is it that prevents mosquitoes from living near these places?

OK , I understand that , but what about spices??                  Do mosquitoes hate it ??

The growing accumulation of experience demonstrates that neem products work by intervening at several stages of an insect's life. The ingredients from this tree approximate the shape and structure of hormones vital to the lives of insects (not to mention some other invertebrates and even some microbes). The bodies of these insects absorb the neem compounds as if they were the real hormones, but this only blocks their endocrine systems. The resulting deep-seated behavioral and physiological aberrations leave the insects so confused in brain and body that they cannot reproduce and their populations plummet.

In case of a regular (house) mosquito, the effects of neem are as follows:
1. Retardation of growth
2. Inhibition of feeding
3. Eggs are unable to hatch
Apart from this, larvae of a number of mosquito species are sensitive to neem. They stop feeding (as mentioned above) and die within 24 hours after treatment.
Studies regarding your question are still in process so it's hard to narrow down to one exact reason.
Sources referred: The National Academies Press

You forgot the reference. The National Academies Press is too vague.

sorry. Here it is: https://www.nap.edu/read/1924/chapter/6


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Origin of logarithmic sense responses?
It's my understanding that most human sensory systems obey an approximately logarithmic stimulus/response curve. This includes the visual system, auditory system, and the smallest perceptible difference on things like weight. Do we know the origin of this pattern? Is it something inherent in how neurons encode information and fire (for example, maybe the refractory period reduces neuron responsiveness to stimulus in just the right way relative to how information is encoded)? Or is it something that specifically evolved to give us the ability to handle a wide range of stimulus amplitudes? If it's the latter, how is the transformation from linear stimulus/response to logarithmic response achieved?

First, the curves are not really logarithmic.
Instead, according to the Stevens' power law, the curves are of the form:
Perceived = k (actual)a
where "a" could be greater, less than, or equal to 1.
When "a" is 1, the curve is linear.
Examples of a=1 (linear), are:
brightness of a "point source briefly flashed"
length perception
cold perception of skin
radiant heat perception
If "a" = 0.5, the curve is a square root curve.  Brightness perception follows the square root (or de Vries-Rose) curve in some intensity regions, and a nearly-linear response in other (Weber's law) regions.
Examples of "a" being positive are perception of electric shock and perception of heaviness of lifted weights.
So, since the perception curves can be linear (a=1), more sensitive than linear (a>1), or less sensitive than linear (a<1), there is no general logarithmic property of neutrons that is responsible for the curves.


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How to run agar gel electrophoresis at home
I've looked at various sites explaining how you can easily make your own gel electrophoresis kit at home. But they always test various food dyes on these home made kits instead of actual DNA samples. Extracting DNA from plant matter can also be done easily at home, so why can't you just run this on the homemade kit?

There are a few reasons why this is usually not suggested.

DNA itself is not visible (at least not in the quantities you'd run on your gel). You need a compound (dye) that binds to the DNA to make it visible, and because they bind to DNA most of these compounds are carcinogenic. Even if you use such a dye, many of them only show up under UV light, an additional difficulty. You could also buy a safe dye that works and is visible, but that makes staining also more laborious. Food coloring will be visible all the time, already when running the gel.
The nice CSI gels you see on TV are showing (supposed) PCR products of short tandem repeats, giving you nice bands at different heights on the gel. These bands also have a convenient size for gel electrophoresis. Restriction analysis of plasmids is also something you'd see more often, and also here the pieces are between 100 and 10,000 bp. DNA extracted from plants consists of genomic DNA, huge strands (millions of base pairs) that will not really run on an agarose gel. Getting a selection of discrete-sized DNA fragments is really not so easy in your kitchen, that's why they go for food dyes.


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Books for learning how plants function
Can you recommend a good, detailed book on how plants function? A book that explains plant processes on a molecular level from roots up to the fruit.
I am interested in home crops production, such as tomato and peppers, but I expect the principles to be the same for most of the plants. There are lots of "how to garden" books, but this books don't explain things, they just tell what to do.
Background: I have a degree in chemistry so I am confident in my knowledge of chemistry and chemical analysis. But this knowledge is useless unless you mixed it with other science branches, such as biology.

I think you would need a plant-physiology book and a biochemistry book.

I wanted to comment because I don't think my answer will be the best, but I can't because of my low reputation... Anyway, here are two suggestions:

Plant Physiology and Development, by Lincoln Taiz, Eduardo Zeiger & al.
Biochemistry and molecular biology of plants, edited by Bob B. Buchanan, Wilhelm Gruissem and Russell L.Jones

These are the two main books we are using in my university (I'm studying biology) and I think that together they cover a lot of topics. You can probably buy the pdf versions online as well. I hope it helps!

Buchanan and Jones is probably the most recommended (and  very detailed) book in that stream.

As user @Tyto alba said, the stream you are telling about, is called plant physiology; so you would need some plant physiology textbook.
For a general account on all aspects of plant physiology, and where the plant metabolisms are specialized than from animal metabolism; a very good book is
Plant physiology by Lincoln Taiz and Eduardo Zeiger, Sinauer publication.
 (cover picture from here).
There are ample changes in different editions, we commonly used the 3rd and 5th edition.  There are more current editions too.
Google books link, Ed-5 content (pdf) by Sinauer , Ed-6  in official website of publisher, and currently active companion website for 6th edition.

The 6th edition have a changed title, "Plant physiology and development", with addition of more authors Ian M. Møller, and Angus Murphy.
................................................
For a basic, student-friendly book, Visit Introduction to plant physiology by Hopkins.
.
The book is very much conceptual, the language is lucid, and there are many helpful illustrations in line drawing.
There are Newer editions of this book, assisted by N. P. Huner.
Google book link to 2nd Ed content, All editions, Publisher website (Willey) official link.
.................................................
For an encyclopedic account, covering all aspects of plant physiology,
Visit Plant physiology by Salisbury and Ross.

Link to Google book 4th Ed,
Publisher: Wadsworth Publishing Company. (No mention of this book on website curently)
Link on Amazon and Flipkart.
...............................
For more detailed biochemical aspects: (also for the basics of applied metabolic chemistry for crop production)
Plant biochemistry, by Hans Walter Heldt, assisted with Fiona Heldt, Elsevier

The original book is in German, but English-translated edition is popular worldwide.
Also available under heading, "Plant Biochemistry and Molecular biology".
A standard basic textbook, very-much conceptual, as well as student-friendly. Contains lot of detailed diagram and Sketches.
Publisher (Elsevier) Link to 3rd Edition, 4th Edition
..............................................
Another wonderful book, for basics in details, is
Plant Metabolism, edited by Dennis, Turpin, Lefebvre and Lyzell.

Publisher: Longman ( Pearson )


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Function of the spermaceti organ
What is the use of the spermaceti organ of the sperm whale?
One possible theory considered is that it was used for floating and going underwater by heating/cooling the oil. However, it is a lot easier for this to be done mechanically.
Another possibility is that it is comparable to a helmet to safeguard it when it collides with another whale. However, other animals have much simpler structures to deal with this problem.
A third possibility is that it uses it to stun its prey like squid. However, research in inconclusive on whether squids can hear or not. The link below, says that it is probable that squids can only hear upto 500 Hz which is not the frequency used by whales, thus this theory is probably false as well.
https://www.treehugger.com/natural-sciences/what-can-squid-hear-and-why-does-it-matter.html

It would be better to link(cite) your first and second hypotheses by peer-reviewed articles.

The principal function of spermaceti and the associated structures in a sperm whale head, is echolocation. The composition of spermaceti suggests that it functions as an acoustical transducer, helping to focus the powerful sound waves used for echolocation. These sound waves likely do not actually stun squids, but they do help sperm whales to find and pursue squids in deep, dark waters.
An echolocation click is formed at the tip of sperm whale's nose, where it is directed backwards, through the spermaceti, toward the sperm whales brain. It then is reflected off an air sac on the sperm whale skull, and redirected forward through a series of lenses before it moves into the water. Check out an illustration of this in the Møhl et al 2003 paper: https://pdfs.semanticscholar.org/88d4/271e9f7490c1173234a2445cf8ddf92fd51f.pdf
The complicated anatomy in a sperm whale's head seems to be directly evolved for echolocation.
Sources:
Karol, R., Litchfield, C., Caldwell, D.K. et al. Mar. Biol. (1978) 47: 115. https://doi.org/10.1007/BF00395632
Møhl, B., Wahlberg, M., Madsen, P. T., Heerfordt, A., & Lund, A. (2003). The monopulsed nature of sperm whale clicks. The Journal of the Acoustical Society of America, 114(2), 1143-1154.

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Thermophilic yoghurt bacteria survivability in the gut
Would they mostly not simply perish since they need much higher than body temperatures to thrive? Are mesophilic ones (such as kefir) much better at that and thus have better probiotic functions?

I had magnesium supplements for a while because i was deficient, but their alkaline pH upset my gut and I had gas. Afterwards, I tried all kinds of cheese and yoghurts, olives and whatever fermented food i could find. They had nearly zero probiotic action. one day i had fermented taboulet salad from a pack that had puffed up from fermentation. I was completely better for a week, Since then i decided that cheese has very little probiotic effect and that a soup that was purposefully left on the counter for days until it goes biological has incredible probiotics.

Milk contains no cellulose and plant matter, so if you eat plants, a fermented equivalent of milk, unpasteurized/fermented plant matter, should logically provide probiotics more adapted for humans. Milk products are a good contribution to diet but it's a myth that they are contain a suitable mix of probiotics for all people, they are probably most effective for digesting protein. cheese yeasts can thrive between 0-43 degrees and diverse cheeses contain a bigger diversity of species.

I have been questioning the usefulness of commercial yoghurts stored, sold and served chilled. And @comprehensible, your point well taken, unless there is a lactose and caesin rich diet, these poor mircrobes will only starve and suffer in the gut if they had not already died of cold.


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Elastic arteries and muscular arteries supplying to upper body
What are the elastic arteries and muscular arteries supplying blood to upper body (above heart) in humans?


text:
Why don't neurons die during a stent procedure in the brain?
Stents are used to provide scaffolding to the blood vessels. When they are used in arteries or arterioles in brain, won't neurons die because of lack of oxygen during procedure?

I am assuming you are asking because of occlusion during balloon angioplasty. If not, please clarify.
Ischemic stroke occurs when a blood vessel to the brain is occuluded by a clot or some other emboli or poor perfusion due to atherosclerosis (a type of narrowing of the vascular lumen). Given enough time, ischemia can produce tissue death, called infarction. It is possible to suffer an ischemic stroke (or ischemia to any tissue) without substantial infarction if reperfusion occurs quickly enough.
Time to tissue death
For stroke, the catchphrase "time is brain" is often used to indicate the importance of occulsion time in stroke. Cell death is not instant upon loss of oxygen, but rather occurs throughout any extended reduction in blood flow as well as during reperfusion.
The brain is more sensitive to ischemia than other tissues like the heart, but there is still a window in which little to no damage is done. By 5 minutes, however, neuron death can begin.
Balloon Angioplasty
When using balloon angioplasty (including during balloon delivery of stents), a single vessel is occluded for ~30-180 seconds. It is also possible for multiple individual inflations. Importantly, this time range is normally kept less than the ~5 minute range for damage to occur.
Embolic protection
One of the dangers during balloon angioplasty is the release of particles from the vascular wall that is being opened up. Those particles can cause distal embolisms. In other organs like the heart, this problem is fairly minor, because only small amounts of myocardial tissue are expected to be impacted which will not have a major impact on heart function. However, loss of small regions of brain could have significant impacts on patient recovery. Therefore, embolic protection strategies are sometimes employed which include devices to block distal flow or capture emboli. The use of these devices is very case-dependent, because if there is already a significant blockage it may not be possible to use particular devices for a particular case.
In any case, pharmacological protection with drugs like aspirin and clopidogrel are standard for interventional angioplasty procedures.
Balloon alternatives
Balloon-mounted stents are standard for coronary procedures, but in the periphery, including carotid and neurovascular implants, there are other stent types, such as nitinol, a shape-metal alloy of nickel and titanium. These are also known as self-expanding stents. They are deployed by removing a protective sheath and they open up on their own. Thus, there is no total occlusion during a nitinol stent deployment. However, balloons can still be used with nitinol stents to open up the original blockage, because the nitinol stents themselves don't "push" nearly as hard against the walls.
In my opinion, the major benefit to nitinol stents is not that occlusion isn't necessary for their deployment, but rather that they are not sensitive to crushing. With a regular stainless steel stent, external pressure would permanently deform the stent. In the heart that isn't a problem, because if someone is poking you in your myocardium you have bigger problems. However, the carotid arteries are fairly exposed in the neck, and a regular metal stent in the neck could be compressed and deformed. Instead, nitinol will snap back into position, like the underlying tissue.
Neurovascular circulation redundancy through collaterals
Although any ischemic tissue can eventually develop collateral circulation pathways to bypass the occlusion (assuming partial and not total occlusion, sufficient to keep the tissue alive in the meantime), the neurovascular system is unique for the high degree of redundancy present even in normal individuals with no blockages. Therefore, occlusion of a single vessel even permanently may not cause substantial symptoms. Of course this will vary from patient to patient and depends on the patency of collaterals, overall vascular health, and specific anatomy at the site of treatment.
Caveats
Of course there are risks in any surgical procedure. It is unlikely that there is zero neuronal death during any neurovascular procedure. Rather, these procedures are used when there is already significant risk or imminent damage without intervention; the intent is to create as little damage as possible while either solving an acute problem that is much worse, or reducing the likelihood of future infarction events.
References
Kulik, T., Kusano, Y., Aronhime, S., Sandler, A. L., & Winn, H. R. (2008). Regulation of cerebral vasculature in normal and ischemic brain. Neuropharmacology, 55(3), 281-288.
Lee, J. M., Grabb, M. C., Zipfel, G. J., & Choi, D. W. (2000). Brain tissue responses to ischemia. The Journal of clinical investigation, 106(6), 723-731.
Mousa, A. Y., Campbell, J. E., AbuRahma, A. F., & Bates, M. C. (2012). Current update of cerebral embolic protection devices. Journal of vascular surgery, 56(5), 1429-1437.
Pan, Jie, et al. "Reperfusion injury following cerebral ischemia: pathophysiology, MR imaging, and potential therapies." Neuroradiology 49.2 (2007): 93-102.
Saver, J. L. (2006). Time is brain—quantified. Stroke, 37(1), 263-266.
(disclaimer: I worked for a major manufacturer of intravascular catheters and stents for about 4 years. I was last employed by that company ~8 years ago and no longer have any financial relationship with that company. Everything in this post represents my own personal views. I am not a medical doctor; this information should not be taken as medical advice. Only your doctors/interventionalist can give appropriate medical advice according to your specific case)


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Does hunger necessarily mean that we should eat?
People feel hunger sooner after they eat food that consists mostly of carbohydrates. For example, if someone eats a good portion of rice then most likely they will be hungry after a couple of hours. But should they eat again in such a case or is it just deception because of blood sugar hikes?


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What is this bee/wasp nest?
Perhaps this is a tropical wasp. Can you identify it? Is it artificial?

What is your location? Also, what makes you think that this is a wasp nest?

Sorry, I dont know where it's from: I was researching animal nests, and I found the pic on a random trivia page. Then I searched google images, there are only 3-4 HD copies of the photo and I couldn't find the origin of it.

FYI this appears to have originated from reddit user Crabcaked from this reddit post. I added more pictures to your question here from that post

I do not believe that this is a wasp nest. What makes you think that this nest belongs specifically to a wasp species?

awesome, well spotted. I thought that reddit was joke website. I wrote that it was a wasp because the web page was called "strange places to find a wasp nest" and had household objects surrounded by nests and things.

This is likely a honeycomb created by some species of honey bee.
A beekeeper (Jessie Brown) from New Mexico shared to her blog the following photos of a "free form" bee hive some of her bees created:

 Photo credit: Nina Dubois
In that instance (as well as the one mentioned here and pictured below), the beekeeper moved some "burr comb" to a new location and the bees used that moved remnant piece to build a mound-like comb.

 Photo credit: Phillip Cairns

That is pretty amazing. Great answer!


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What is the terminal electron acceptor in methanogenesis?
I learnt that methanogenesis is a type of anaerobic respiration that utilizes carbon compounds such as CO2 or acetic acid as their terminal electron acceptor in their electron transport chain rather than using oxygen. However, when I went through my textbook, I found out that conversion of CO2 to CH4 is not one step reaction but many other compounds are synthesized in between and methyl-SCoM is converted to methane.In one article I read that Com-SH is the terminal acceptor When I tried searching in google for the same I came across a lot of diagrams of mechanism but some of them did not match with each other. I have no idea what's going on. It would be really helpful if you can help me out here.


text:
Why is methanol poisonous?
What should we do when someone is diagnosed with the methanol poisoning What harm does methanol cause on our body, such as the harm to some proteins? What first-aid measures should we take?

Are you asking for a real case? Seek help from a qualified medical doctor in a hospital immediately.

This question does not seem of topic to me. I agree that the wording could be better (for instance, "What first-aid measures should be taken" instead of "What first-aid measures should we take"), but OP is not asking for medical advice. She is simply asking: 1. what is the mechanism of methanol poisoning?, and 2. What is the treatment for it?  It's a valid question and @another'Homosapien' already provided a valid, good answer. That being said, I'd vote for reopening if I had enough RP.

@gerardofurtado I counted you in my reopen vote ;)

Related: Chemistry SE

Methanol is highly toxic in humans. As little as 10 ml of pure methanol can destroy the optic nerve and cause permanent blindness,  while 30 ml dose is fatal (Vale et al, 2007). However, its toxic effects take hours to come up after ingestion,  and antidotes are often helpful in preventing permanent damage.
Methanol exerts its toxic effects by two main methods:

Much similar to ethanol, methanol is also a CNS depressant since it enhances the activity of inhibitory neurotransmitter GABA and also interferes with excitatory neurotransmitters.
When ingested, methanol is converted in liver first to methanal by alcohol dehydrogenase, and then to methanoic acid (or formic acid) by aldehyde dehydrogenase (Schep et al, 2009). Under cellular pH,  formic acid exists as formate. Formate interferes with the mitochondrial enzyme cytochrome c oxidase, causing cellular hypoxia and metabolic acidosis (Liesivuori et al, 1991).

To prevent methanol toxicity, two kinds of antidotes are used:

Bicarbonate can alter the metabolic acidosis and potentially reverses the visual deficits.
Ethanol and fomepizole are also used as antidotes to methanol. Since the affinity of liver enzymes alcohol dehydrogenase and aldehyde dehydrogenase is about 10-20 times more for ethanol than methanol, ethanol can thus prevent (or at least delay) metabolism of methanol to formate. During this time, methanol can be removed from the body by kidneys or through dialysis. Fomepizole is also metabolized by the same enzymes, but ethanol is generally preferred due to high cost and low availability of fomepizole (Medscape). Thus, intravenous injections of ethanol can (under some circumstances)  serve as a first-aid measure (although consulting a physician is always the best option).

References:

Vale A (2007). "Methanol". Medicine. 35 (12): 633–4. doi:10.1016/j.mpmed.2007.09.014.
Schep LJ, Slaughter RJ, Vale JA, Beasley DM (2009). "A seaman with blindness and confusion". BMJ. 339: b3929. doi:10.1136/bmj.b3929.
Liesivuori J, Savolainen H (September 1991). "Methanol and formic acid toxicity: biochemical mechanisms". Pharmacol. Toxicol. 69 (3): 157–63. doi:10.1111/j.1600-0773.1991.tb01290.x
Methanol Toxicity Treatment & Management: Medscape


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What is the name for the opening in the mouth for the nasal passages?
Is there a proper anatomical name for the opening in the soft palette where the nasal passages enter the mouth?

Something other than oropharynx?

@skymningen From looking at drawings it looks like I'm talking about where the nasopharynx meets the oropharynx. There may not be a specific name for it. Sometimes openings have their own separate name (like the foramen magnum, or the anus, etc) but not always.

From what I understand from your comment is that you are asking for opening which connects the nasopharynx to oropharynx.
This opening is is connecting two parts of pharynx , acting like a bridge therefore it was named as Pharyngeal/Nasopharyngeal isthmus.
According to this site:

isthmus of pharynx
Type:Term
Definitions
  1. passage posterior to the soft palate by which the nasopharynx and oropharynx communicate (i.e., the junction of nasopharynx and oropharynx), closed during swallowing by elevation of the soft palate and contraction of the posterior fascicle of palatopharyngeus (muscle), forming a Passavant cushion.
Synonyms
  isthmus pharyngis , pharyngeal isthmus

Source of image: Textbook of Anatomy: Head, Neck, and Brain : Vishram Singh


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How can DNA profiling be used to determine the number of organisms from a specific species that is within a certain area?
Here is the tedious exam question that asks this: question 8(b).
https://drive.google.com/drive/folders/0B23NLD5L6099VWJya3dfLVJpbmc
The question states:

In 2007, the brown bear was a threatened species in Alberta, Canada. A study was carried out to determine the number of bears in the area. Fur wascollected from trees that the bears had rubbed against and their DNA analysed.
(i) Explain how DNA analysis would help the scientists to determine the number of bears in the area.

The answer simply states:

idea of comparing bands

idea that each bear has unique {DNA / banding patterns}

idea that the number of different banding patterns would equate to the number of different bears

My question is: How does the entire process fit into together?
I am absolutely baffled as to how the entire investigation would fit into each other, and I've been trying to articulate it for hours. It seems like if I'm just going to be collecting fur samples off trees there are going to be cells belonging to different species, then the DNA pattern produced will include a different number of bands from all of the different species. To overcome this problem, I think 'would we somehow separate the different cells into different groups with each group belonging to a specific bear by some technique that isn't DNA profiling and I don't need to know about at high school level? I then reason that we would have accomplished our task of identifying the number of different number of bears present within the sample. How would one identify the different numbers of bears?
The second part of my question is that I don't understand how the different samples from trees and fur will be used in order to estimate the overall population size within the area? The only animal sampling technique that I know of is that capture-recapture method.

Please just write the question here.

Is it okay now?

The general process of DNA profiling (I prefer calling it "DNA fingerprinting", but that's just me) generally involves developing PCR primers specific for a particular region surrounding some sort of highly polymorphic region. So in this case one would need primers surrounding VNTRs (or other polymorphic regions, have a look at the wikipedia article for an overview of some other methods). Presuming the PCR primers are specific for bears (one could blast them to get an idea of this), then regardless of what other animals were mixed in, the resulting bands would predominantly be from bears (after all, PCR results in an exponential amplification of favored species). This would be answer part (1).
For part 2, one needs to find a sufficient number of sufficiently variable regions for profiling to work. A single site might not be informative enough, but a couple of them together will be.
Part 3 is the logical outcome of parts 1 and 2. If you can amplify a bunch of mixed samples together and the repeats are of variable length (thus the use of VNTRs or similar repeats), then you'll see those as different sized bands on a gel.


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How long before robin no longer needs the nest on my porch?
A robin has made a nest on my porch. Unfortunately, the nest is on my weed wacker which I might want to use at some point this summer. Currently, there are two eggs in the nest.
How long will it be before the robin is done needing the nest?
Location is Eastern Massachusetts.
-- Update May 13 --
I think one of the eggs must have hatched. The robin no longer sits in the nest, she just stands on it constantly.

As cited in my answer, Cornell University Lab of Ornithology's All About Birds website is a trustworthy and excellent website for learning about any bird species across North America (and beyond?). The site contains many pictures and sound clips as well as tons of easy-to-read info about ecology and life histories.

Go to a crowdfunding site, state your concern for the robin's nest, get the cash to buy another weed wacker, everyone wins. Remember to send pics of the chicks to all the donors. If you associate crowdfunding with begging, tell them you are making a presale of robin chicks' photos. Even get some pro photographer from your region involved. Problem solved, nest saved. Donate any excess cash to WWF or any local wildlife preservation charity if you fancy. Post donation receipt online.

As a third option, there are professional bird catchers who can move the next without upsetting the mother too much. That would probably cost more than another weed-wacker though.

@Omegacron I expect the changes of succes to be low.

According to Cornell's All About Birds website, you will have to wait about a month for the nest to be cleared.

The egg incubation period is 12–14 days.
Following hatching, the nestlings will remain in the nest for another 13 days (i.e., the "nestling period" is 13 days).

However, there are two caveats to this:

A typical robin clutch size (i.e. the # of eggs in the nest at once) is 3-5 eggs. Since you only have two eggs, that could suggest that more eggs are about to be laid very soon, which may extend the nest occupancy another day or so.
Some robins use the nest more than once!

An American Robin can produce three successful broods in one year.

Here's a visual of what the nestling period (approximately) looks like so that you can track your nest visually :) :

 Source: L. Birnbaum


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Did some senses evolve from other senses or are they considered independent?
Are there evolutionary connections between different senses, in such a way that one sense is evolved from the other or from a common root, e.g. the possibility that hearing and touch are derived from a common root? If there are such evolutionary paths, are there any attempts to draw a map between different senses?

Hearing and touch are both examples of mechanosensation, i.e. touch receptors are activated by pressure changes and sensory hair cells (hearing) are activated by fluid motion initiated by sound waves. Therefore, I think it makes sense that they evolved from similar origins.
Vision on the other hand is due to photosensation, which has a very different physiology, so I don't think there's any evidence of a similar evolutionary link, but there may be (almost certainly are) similarities in the way our brains have evolved to respond to the different senses.


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How did a plant evolve to know there were animals alive that would eat it's fruit when it decided to produce this fruit?
How did plants come to "know" there were animals alive that would eat it's fruit when it first produced this fruit?

The plant does not "know" there are animals. It is just that plants, that accidentally evolved (due to mutations) a fruit that attracts animals (which can spread its seeds etc.) had an advantage over plants that did not have them. The disadvantaged plants just became extinct after a while. And you must be aware that the first fruits were rather "pre-fruits", but already a selective advantage to their bearers.

How did a plant know there were animals to have have spines, prickling hairs, acidic leaves, soapy sap, stings, wooden seed protection, poisons, and fruit? Same theory.
A fruit is only plant flesh with water and citric acid and sugar in it.
Beetles and lizards also eat seeds and leaves. Even since the first mosses and ferns colonized the planet, the most abundant food was normally forest leaves. So plants "knew" they were being eaten since the times of the first animals because when you get eaten into oblivion, you dont know anything any more:(
All plants contain lots of sugar C6H12O6 in their sap, sugar is very easy thing for the plant to produce. Putting sugar into the seed pod is a easy for a plant as growing hairs from leaf cellulose, growing spines and making stings.
So, plants already had seedpod protection containing acids, poisons, soaps, wood protection like pine cones, and the only necessary change is to go from acid or cellulose, for example citric acid, to sugar, which is chemically an easy thing to do in evolution.
If a mutant tree one day makes a seed pod than some animals like so much, that they don't even break the seeds, then the tree's babies can travel many kilometers and be reborn into an animal nitrate dropping.
Fruit developed independently in yew trees, strawberries, figs, very simply by changing acid or poisonous seed pods into sugar ones that get transported for kilometers in every direction. If a fruit is not sugary, then it has some poisons like chilli peppers, spines like chestnuts, and other seed protection devices.


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How do I download entire human genome for local blast formatting and searching?
I'm trying to make a copy of the entire human genome for local blast queries on my machine.  I understand that I need to download it from the NCBI FTP server here...
ftp://ftp.ncbi.nih.gov/genomes/Homo_sapiens
After downloading it I need to format it into a database that blast can search.  I do this using NCBI's makeformatdb command.  It is run like this...
makeblastdb -in entire_human_genome.fasta -dbtype nucl -title human_genome -out human_genome.db

My question is...  Where do I get the fasta file containing the entire human genome?  Do I download the fasta files for all 22 chromosomes, the X chromosome, and then the Y chromosome and concatenate them?  Is there a fasta file on the site containing the entire genome?  A fasta file that is not partitioned by chromosome?

You can either download and concatenate the individual chromosomes from NCBI or make your life easier and download a single fasta file from Gencode (note that that's the primary assembly, if you want the one with haplotypes then it's here).
Having written all of that, the "human_genomic" files on the NCBI FTP server are the prebuilt blast databases for humans.

Just had a look at the prebuilt blast databases you linked to.  I would want the one named "human_genomic_transcript.tar.gz".  That is the largest one at 6.0 GB.  Is this the complete genome?

You probably want the 21 human_genomic.??.tar.gz files. They each contain subsets of the whole database. The human_genomic_transcript.tar.gz file is a superset of that, additionally containing refseq transcripts. See more details here.


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Book for molecular biology comparative to major taxonomic groups
Want recommendation of books on molecular biology (or molecular cell biology), that elaborately compares the  structures and phenomena in the major taxonomic groups.
For say, whenever studying about a phenomenon ( may it be a structure like ribosome or nuclear DNA or plasmid or small RNA or nuclease enzymes, or may be phenomena like central dogma (replication, transcription, translation) or recombination or cell-division and its regulation, or may be protein folding or protein degradation, or biosignaling pathways)... I could get the analyses about in detail the similarities and the differences of the processes in different taxonomic groups.  Such as, How does that process happen in prokaryotes (both archaea and eubacteria) and eukaryotes? Or if further zoom-in; how the process varies in major group of archaea, bacteria(Gram-positive and Gram negative), protists, animals (invertebrates and vertebrates),  plants(bryophytes, pteridophytes, gymnosperms, angiosperms), or fungi (glomeromycetes,ascomycetes, basidiomycetes etc)? or how the processes takes place in the mitochondrial and plastidial genomes of the different groups of organisms?
Best if the book could provide ample amount of data tables.
There are books and articles specific to a few certain taxonomic groups; but I'm looking for the big picture or the bird's eye view.
Thanks in advance.

I doubt you'll find one. It would be a huge amount of work, it would be out of date immediately, and only three people would buy it. The days of printed catalogues of this type are long gone. The cheap updatable internet put an end to them. Even the "Where to Ski" book has sadly gone online.


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Understanding the picture of a synapse
I need help to see exactly what is going on here. According to the textbook here is shown a synapse, but I cannot quite see the things the textbook says are there.
From what I understand: (1) At1 and At2 are axons?, (2), The black thing on the bottom left is a dendrite?, (3) s1 and s2 are post-synaptic densities?
Is there more to see here that I am missing?

The word is "synapse" not "synapsis" - and yes, those are the major features to see. Note that is probably more correct to say those are axon terminals, hence the "at". All the spherical objects inside the axon terminals are vesicles. I think this question should probably be closed, though, because you don't have much of a question: the textbook is telling you what's in the picture.

Does the book have another diagram or picture of a synapse from a different angle? Or a picture that shows synapses within a larger context? Would be worth adding to this post if so.

You can tell that the structures labelled At are axons, or rather axon terminals, due to the presence of the synaptic vesicles.
I think this is a fine photo that's a bit more a clear representation:

Source
PSDs are really just protein aggregates that are thought to facilitate neurotransmitter trafficking. So the structures here make sense. At least, they make sense if you know the tissue you're running in TEM, and you understand that how you cut the samples for microscopy affect the way they end up looking. My only assumption that Den is a dendrite is knowing that axon terminals synapse with other dendrites: they're receiving structures. I'm also somewhat sure the cell body from which the dendrites extend have that characteristically large nucleus.
The other understanding is that these pictures are just snippets of a larger image and you only get used to identifying structures through practice and experience. Rather, the author wants you to see this section and for lack of context has identified the structures for you.


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During interphase, is DNA wrapped around histones?
Are histone proteins present around DNA in the nucleus during all of interphase (including G1) or do histone proteins only form later on when chromosomes are condensing into chromatids?
Thanks in advance!

Yes, DNA is always wrapped around histones.
DNA condensation using histones is not only meant to form the chromatids for mitosis/meiosis, but also one of the factors that control gene expression. Tightly packed heterochromatin is not being expressed, whereas unpacked euchromatin is transcriptionally active. The process of condensation is controlled by enzymes such as histone actelytransferase (HAT) and deacetylase (HDAC) that change the electrostatic properties of the histone proteins. Positively charged lysine in heterochromatin histones allows condensation with negatively charged DNA. By acetylation of these lysines, they become neutral and the heterochromatin turns into euchromatin, which, provided the necessary activators etc., can now be translated. To silence gene expression, the process is reversed.
Gene expression control is very complex and histone acetylation is only one factor out of many. Nonetheless, you see that histones are a crucial part of the chromosomes and are not only formed during mitosis or meiosis.
3.0.jpg
Source: https://en.wikipedia.org/wiki/File:Histone_acetylation_and_deacetylation.jpg


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Is the skin of feline jungle predators protected against ants?
I was watching a video of a jaguar stalking along a riverbank, killing prey, climbing up the muddy bank, then laying in thick brush to eat. My first thought about this is that there must be tons of ants. I've never been to a jungle but on muddy river banks around where I live if you crawled around near the water and on the forest floor in general you'd be sure to get attacked by ants and it would result in hundreds of bites which cause swelling, major discomfort, and perhaps infection.
This seems like it would be a problem for large mammal jungle predators that kill prey in that kind of river bank area and then plop down and eat it. Does the fur make them immune to ant bites, or ants more rare in the jungle than I imagine, or they do get bitten but they just have a high tolerance for pain?


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Why do sparrows jump instead of walk when they are not flying?
I want to talk about sparrows, one of the most common birds around the world. I noticed that when one slowly walks into them (so that they are not frightened enough to fly away), these tiny birds would jump away, rather than walk away, as if they are not able to walk.
Why?

This is the first result I've got in Google: "As for why sparrows jump, I suspect that they are perfectly capable of walking, but find hopping to be a more efficient way of moving across the ground in the irregular pattern that they generally prefer. This is partly a function of their small body size, since jumping is typically easier for small animals than for large ones of the same approximate shape." C Sullivan, Institute of Vertebrate Paleontology.

Also, there is a good explanation here: https://www.theguardian.com/theguardian/2010/jan/27/some-birds-hop-others-walk

That’s the way God made them.

As pointed out by @jamesqf in the comment below, there exist many birds like quail and pheasants that run and walk rather than hop. Also, there are several flightless birds like  ostriches, emus, rheas that do the same. But it is also true that sparrows don't walk or run but hop. The question now is- why?
There is an interesting fact- both Quail and Pheasant are ground nesting birds.
Now, the reason why we do not see sparrows running like pheasants is because sparrows rely more on their ability to fly for survival and getting around. So, a sparrow will rather fly the distance than run. The reason for this might be its smaller size which makes it more efficient and safe during flight.
But the question is- why don't sparrows walk? Why do they hop? Quails (video) and Pheasants(video) certainly walk even for short distance.
Just before a flight, all birds jump to power their flight. So, if a sparrow hops around rather than walking around, it can convert any of these jumps into a full flight in the case of an unexpected need. This again comes down to sparrow's heavy reliance on flight to escape danger. Because of their light weight, hopping rather than walking is less costly for a sparrows.
Whereas in a normal situation, Quails and Pheasants would rather run to build the necessary  momentum to initiate a flight. But they walk even for shorter distance because they are heavier than a sparrow, and walking for them is more efficient than hopping. But in worst case scenario, even birds like Quails can simply jump into a flight, as can be seen in this video if you watch it in slow motion.
Edit: another factor that might influence whether a certain bird hops or walks is the irregularity of the terrain with respect to the size of the bird. The terrain is relatively more irregular for smaller birds (there are obstacles like twigs, stones, grass etc), hence making hopping a better option than walking.
There are many kinds of birds that each choose whether to walk or hop. Here i present a small categorization with video evidence to bring out some pattern if any. You might need to watch some of the videos in slow motion.
Birds that hop:

sparrows
American robin
blue jays

Birds that walk

Crow
magpie
Quail
Pheasant
an unknown small bird that the video title says is American robin but which walks

You have a very long answer, but very little of it answers the main question. This is ok, except that your actual answer is not supported by any citations or links to sources. Please [edit] your post to include support. Thank you

Comments are not for extended discussion; this conversation has been moved to chat.

An avian researcher states that birds with short necks hop as it allows them to turn around faster and benefits their 360' field of vision so it aids their agility and perception, wheras walking birds have longer necks and can see around them while walking.
https://www.researchgate.net/publication/264193094_Biped_gait_in_birds_some_observations
https://www.researchgate.net/publication/233934125_Hopping_in_Birds_is_The_Choice_of_Gait_Influenced_by_Cervical_Mobility_and_Field_of_Vision
Perhaps walking distracts vision for animals that can't bob their heads like pigeons, the stiller the eyes are, the clearer the peripheral vision.
As pro ornithologists states that birds that are adapted for tree life and constant branch hopping also hop around on the ground, however birds that spend a lot of time on the ground save energy by walking.
https://ww2.rspb.org.uk/birds-and-wildlife/bird-and-wildlife-guides/ask-an-expert/previous/hop_or_run.aspx


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What is the name of this plant with mango type leaves?
Location: South India
Leaves: Mango Type
Indoor/Outdoor/Wild: Indoor
Month: May

This looks very much like a plant in the Ericaceae family, and specifically it looks to be some species of rhododendron.

Shrubby looking tree/shrub
Spirally arranged stiff (appears evergreen) leaves
Strong midrib on leaf
Large flower

With over 1000 species worldwide and more than 120 species known to occur in India, the picture likely doesn't have enough detail for someone without specific knowledge of Indian plant species to be able to ID to species. Even an expert might need the following details:

Exact leaf measurements, specific habitat details (elevation, distance to water, etc.) and closeups of leaf undersides, stem axils, bark and (opened) flower. A zoomed out picture showing the whole shrub/tree would also likely be helpful in IDing to species.

I would recommend reading Mao (2010) The genus Rhododendron in north-east India.

List of species and locations etc.

 Disclaimer: I am not very familiar with Indian flora, so I could be unaware of genera/species that might be a better fit. Please try using a flora with dichotomous key to ID.


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Difference between bacterial chlorophylls
I understand that bacterial chlorophylls are of the form a, b, c and d.
But i read in my textbook about pigments like bacterio purpurin and bacterio viridin; are they a part of the 4 types of chlorophylls and if not how are they different and what actually are they?

What research have you done before asking it here?

@another 'Homo sapien'  i looked through a couple pages on the internet about bacterial photosynthetic pigments along with a wikipedia page and also a couple books but none of them were very clear about the relationship between bacterio purpurin/viridin and bacterio chlorophylls.  Thus,  my question is simply to ask for the relationship between them and if someone could explain the difference between

Thanks for the question... me too unfamiliar with the term "bacterio-purpurin", however only recall the term "bacterio-viridin" in my old middle-school textbooks in context of photosynthetic pigments. I can't recall I've seen the terms anywhere else. Maybe they are obsoleted terms now replaced by some other terms. I'm not seeing these 2 terms in wikipedia, too.

From A search in Pubchem database, in substances for bacterioviridin, it seems just another synonym for bacteriochlorophyll-C.
.
The incomplete page do not show any image-entry. From another entry about bacteriochlorophyll-C, I've took the following image:

Bacteriochlorophyll-C; which is being told same as Bacterioviridin
...............................................
...............................................
From similar search on same website for bacteriopurpurin, it shows,

Bacteriopurpurin

is a Xanthophyll compound; with another similar entry Bacteriopurpurin
It is also being called Hydroxyspirilloxanthin
....................................

Another search reslult, Bacteriopurpurin 18,

shows this photo:

Which is clearly a porphyrin-type compound (With smaller 4 pyrrole-type rings) with nitrogen (N) atoms.
......................................
......................................
Though you have not mentioned in the original question, another such old term is Chlorobium-chlorophyll. When searched ;  there i could found one entry in the PubChem database, about chlorobium chlorophyll; which tells; it is same as bacteriochlorophyll-D, though the incomplete page does not display any structure.
From some other entry about bacteriochlorophyll-d; the structure given here:

Bacteriochlorophyll-D, which is being told same as chlorobium chlorophyll. Look this has a little bit different structure from bacteriochlorophyll-C (bacterioviridin according to pubchem) , because chlorophyll-D (this) is lacking a methyl group at left hand middle side of the photo.
................................................
However, I cannot ensure they are free from nomenclatural conflicts. IMO it is better to use modern terms like bacteriochlorophyll-a, b, c, d, e, f and g.
................................................

Reference: The PubChem Project by NCBI

.....................................
N.B. :
To quickly find differences among some main types of chlorophylls and bacteriochlorophylls; I've attached the following diagram. Most of the pictures are taken from PubChem; two I couldn't found in Pubchem, so I took them from a PMC articles. All are linked below the diagram.

Comparisons among some chlorophylls and bacteriochlorophylls.
Sources:

Chlorophyll-A : PubChem, Wikipedia .
Chlorophyll-B : PubChem, Wikipedia .
Chlorophyll-C1 : Pubchem (PubChem also tells as "Chlorophyllide C1") .
Chlorophyll-C2 : Pubchem (PubChem also tells as "Chlorophyllide C2") .
Chlorophyll-C (C1, C2, etc): Wikipedia .
Chlorophyll-D : PubChem, Wikipedia  .
Chlorophyll-E: No records seen.
Chlorophyll-F: PubChem .
Chlorophyll-F ' : PubChem .
Bacteriochlorophyll-A :  PubChem .
Bacteriochlorophyll-B : PubChem .
Bacteriochlorophyll-C : PubChem (Bacterioviridin) .
Bacteriochlorophyll-D : PubChem (Chlorobium chlorophyll) .
Bacteriochlorophyll-EF : A PMC article * .
Bacteriochlorophyll-FF : same PMC article * .
Bacteriochlorophyll-G : PubChem .

The PMC Article * : Bacteriochlorophyll f: properties of chlorosomes containing the “forbidden chlorophyll”, by Vogl, Tank, Orf, Blankenship, Bryant.
.....................................

thanks for taking the time to go through pubchem,  but as it seems bacterio purpurin is still doubtful and do you have any idea about a similarity between chlorobium chlorophyll and bacterio viridin,  are they synonymous?

Not showing synonymous. I've started already adding info about chlorobium chlorophyll

@AnamikaGhosh Thanks very much for asking the question... otherwise the fact behind some mysterious terms would remain unknown to me.

So, what's the conclusion here? Is bacteriopurpurin a type of bacteriochlorophyll?

According to the PubChem entry Bacteriopurpurin can't be a chlorophyll. It has a different structure.


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What determines when plants grow?
I am interested in dryland ecosystems, and I am trying to find material on what determines the time at which plants in dryland ecosystems, either shrubs or grasses, grow and shoot? Is it only related to water availability? Is temperature also a factor?

Plants are not sentient beings and do not know anything. Please phrase your questions in scientific terms.

Metaphoric language that I meet here and there (http://www.whataplantknows.com/)

Best avoided. Making your words reflect and clearly communicate your thoughts is part of being a scientist.


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Arteries used for inserting catheter
For catheter purpose, femoral and subclavian arteries are mostly used as starting point. Why? Are there other arteries which are used for the purpose?

What research have you done? What aspect you didn't understand?

research - "For catheter purpose, femoral and subclavian arteries are mostly used as starting point."

What have you searched regarding your question?

depends on the purpose that you're talking about... we insert catheters for hemodynamic monitoring into the radial, brachial, femoral arteries. For other percutaneous methods, other arteries could be accessed, but less commonly - depends on what purposes your talking about

Those arteries are (a) big enough for the catheters, (b) superficial enough (close enough to the surface of the skin) for catheterization. It would be quite a challenge to use the renal arteries, for a ridiculous example. There is also less of a risk of embolization than using an artery like the carotid, where embolism can cause stroke, which would be quite serious. An embolism in an arm or leg could be painful and cause damage, but unless it is massive it isn't going to significantly affect the patient over the long term.
Also note that those are fairly special cases of catheterization, such as when doing percutaneous interventional techniques targeting the peripheral or coronary arteries. Those approaches use fairly large devices so you need a large vessel, and you need to be in the portion of the vasculature that you are targeting (i.e., you can't access those targets through a vein). As @VanceLAlbaugh mentioned in a comment, other arteries are targeted for other purposes. And overall venous catheterization is much more common than arterial, such as when an IV line is established to deliver fluids/medicines.


text:
Homework question on chemically defined medium
Why would the following medium not be considered a chemically defined medium:
Glucose, 5 grams (g); NH4Cl, 1g; KH2PO4, 1g; MgSO4, 0.3g; yeast extract, 5g;
distilled water, 1 litre
I am unsure why it is not a chemically-defined medium considering all measurements and grams are given and such is required for it to be one. Therefore I am unsure why it would not be a chemically defined medium.

Welcome to Biology.SE. Your question appears to be a homework question that is considered off-topic on this site, unless you show attempts to answer your question. Please edit accordingly and give information about what you think could be a possible answer and people will be glad to help you. Additionally, please edit your title so that it gives an actual question. Otherwise your question will very likely be closed and left unanswered. Thanks. :)

Please read this before posting homework questions

Agree that this should be closed as homework, but I'll give a hint: Look at all the ingredients. Do you know precisely what each and every one is, chemically? Or is there at least one ingredient that is more ambiguous...

@canadianer And I thought my hint was too obvious :-P

@BryanKrause Haha sorry, I didn't read your comment all the way through.

For what it's worth, I think the subsequent edit by the OP shows sufficient effort for this question to remain open. I think it's clear where their confusion comes from.

I think a good example of, well, what is a chemically defined medium is helpful here (RPMI 1640).

A chemically defined medium is, according to this Wikipedia article:

... a growth medium suitable for the in vitro cell culture of human or
  animal cells in which all of the chemical components are known.

Four of the five components fit this criterion precisely, as they are chemical formulae (and of course a common name for a compound whose formula is well known).
However, even though you know exactly how much yeast extract was added to the medium, you do not know its exact chemical composition. To be sure, assays of the chemical composition of yeast extract have been run, and one could come up with approximations of it's makeup. But the bottom line is that there is no precise chemical formula for yeast extract as there are for the other components of the medium.

it does make a bit of a difference :)

The yeast extract would consume and metabolize some of the medium components and metabolic products will be formed. This new introduction of products by the yeast, whether waste materials or otherwise, is unaccounted for and changes the composition of the medium. Therefore, it would no longer be chemically defined.

This is wrong. Yeast extract is prepared from yeast cells by removing cell walls, see here.


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Can I just simply exchange the eyepiece in a microscope?
I hope it's the right place to ask about microscopy. So my question is what parameters do I have to take into account when buying a new eyepiece for my microscope? Currently I own an Aomekie XSP-42 with a WF16X eyepiece and I would like to upgrade it with a WF25X eyepiece. However when I was searching for one I couldn't help but notice that only the magnification and the mounting size are indicated. What about other parameters (eg. focal distance)? Are they standardized or they just simply don't matter?

Did you try to contact the manufacturer?

No, not yet. So it is product dependent if its possible or not?


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Exact definition of 'convergent' and 'divergence' in cell signalling?
From what I understand, we refer to 'signal convergence' as being when two different ligands/stimuli lead to the same (at least in part) responses inside a single cell. This may or may not be due to activation of the same pathway, so for example we can refer to the response of a muscle cell to adrenaline and to stimulation by the nervous system via acetylcholine as convergent because they both lead to the release of calcium. We can also refer to the activation of the phosphoinositide pathway by both activation of beta phospholipase C via a heterotrimeric Gq protein, and activation of gamma phospholipase c via the tyrosine kinase pathway, as signal convergence.
So it seems to me that 'convergence' is defined on the level of the cell with it being, in a nutshell, different stimuli resulting in the same effect regardless of at which point in some internal signalling pathway the two responses 'converge' (at least in part).
Now with divergence I am getting slightly more stuck, and I have not seen a single, clearly stated, definition. Firstly, does divergence refer only to the level of the cell, or also for the whole organism? In particular, I am thinking of cases where a single ligand has different responses in different cells, such as adrenaline leading to increased contraction in muscle cells and glycogen breakdown in the liver (I know this isn't the best example because adrenaline technically leads to glycogen breakdown in both cell types).
Perhaps instead divergence is only referred to on the level of the cell, as with convergence? So for example generally tyrosine kinase stimulation activates several different proteins, which trigger different responses: ras, gamma phospholipase C etc. Even the phospholipase C pathway produces DAG and IP3, which have different responses. But then it seems to me like practically all pathways are divergent if this is the case, because generally pathways lead to several responses inside the cell. So with the case of phospholipase C which cleases PIP2 to DAG and IP3, the DAG can regulate metabolism and transcription etc via protein kinase C and the IP3 leads to calcium ion release that causes muscle contraction. Would this be referred to as divergence?
I would greatly appreciate if someone could just state what exactly convergence and (especially) divergence refer to. I am relatively new to cellular and molecular biology.

In my experience those terms are primarily used intracellularly, but I wouldn't argue that it is wrong to use them more broadly, it's just that essentially everything released extracellularly is going to have some level of divergence, so it makes more sense to use a separate classification scheme (i.e., endocrine/paracrine). Between cells, the terms are also used in other contexts such as the nervous system to refer to inputs from multiple neurons synapsing on one neuron (convergence), and outputs from one neuron synapsing on many targets (divergence).
Convergence just means multiple signalling pathways converging on the same target: like multiple pathways that can activate phospholipase C.
Divergence just means that one effector, which could be a protein such as a kinase or a second messenger like IP3, has multiple targets.
You are quite likely to get both convergence and divergence within any given signalling pathway. In my opinion, this is one of the ways that biology is not taught well in schools: textbooks might make it seem like convergence and divergence are these concrete, specific classifications, but they are really just descriptive terms. Phospholipase C pathways are a great example that displays both. If you are talking from the perspective of activation of phospholipase C, you are probably talking about convergence because there are so many ways to activate phospholipase C, but at the same time, if you talk from the perspective of the G protein subunit that is activating phospholipase C, that G protein probably has other targets as well, so that's divergence. And downstream of phospholipse C you have divergent effects of DAG and IP3.

Ah, I see. I like how you stated that convergence and divergence are 'really just descriptive terms'- it makes a lot of sense; in any pathway you can probably find a point at which several different inputs can activate a certain protein or have one given effect, or a single protein will have several different effects- divergence. A whole pathway itself won't just be an example of convergence or divergence.


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What is the resistance of a single human cell?
What is the resistance of a single human cell? I know different cells will have different values, some examples would suffice. I did not find any such information on the internet.

At what voltage? Not only does this differ by cell (and environment), it often varies by voltage (and time due to inactivation).

Welcome to SE Biology. Please insert the term "electrical" in your title and question to make it clear what you are talking about. It would also be a good idea as a new user for you to complete the tour, your lack of the badge for that implies you have not.

Hi poi. Welcome to Bio.SE. Please clarify which type of resistance you are referring to. Also, we ask that you demonstrate some previous effort on your own part to have answered your own question. Please provide such support. Thanks.


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In SDS-PAGE, why are the sample buffer and running buffer different in concentration?
I'm currently trying to understand the concepts of SDS-PAGE. Every protocol I've read says to use 5X for sample buffer and 1X for running buffer, but I don't really understand for what reason? What are the negative consequences if I don't?

Please give the composition of your buffers. You can't expect us to know what they are and if we don't we can't give an answer to your question that is of use to anybody.

The reason why the sample buffer is more concentrated (typically 2x or 5x depending on your protein concentration) is its dilution when you mix it with the sample. You mix 4 parts of your sample and 1 part of 5x sample buffer, so that the final concentration of this buffer is 1x.
If you use 1x sample buffer together with the same amount of sample, the final concentration of the sample buffer would be 0.5x, if you do the same 4+1, it would only be 0.2x in the end.
This dilution is too strong and the buffer will not fulfill its purpose, the complete denaturation of all proteins in the sample, so that their distribution on the gel depends only on their molecular weight and not also on their tertiary/quarternary structure.
Using a 5x buffer allows you to add a lot of sample when diluting it to 1x without changing the concentration of the protein too much. It also allows to load larger amounts of sample compared to 2x buffer, interesting when the protein concentration is low.
The running buffer is not further diluted by adding sample, so that it has to be diluted to 1x in order to have the right ionic strength. Since these are often used in big quantities in the lab, it is more convenient to prepare concentrated buffers in smaller quantities and dilute them before usage than preparing big tanks of buffer.

Worth adding that the reason for using e.g. 5x sample buffer is so that the sample can be brought to 1x without greatly increasing sample volume and thus decreasing protein concentration. In many situations you may want to load as much of your sample protein as possible in the well.

@AlanBoyd Good point. I do this often but don't think too much about it anymore :-)


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What types of plants are Gibberellin used on?
On what type of plant (monocot/ eudicot? family? species?) is Gibberellin used on?
I searched through many sources but could not find whether Gibberellin works for all plants or just a specific type or family. I read that it works well for biennials, but what are some of the other plant families that it is useful for?

I don't know what you mean with 'used on' but gibberellins are plant hormones in ferns, monocots and dicots. All of these plants will react to the application of gibberellin but the effect will depend on the dose, type of molecule and tissue where it is applied. All plant hormones have multiple effects but the classic one for gibberellic acid is stem elongation.
Too much of this can kill the plant though as is the case with Bakanae fungus infection which forces the plant to overproduce gibberellic acid which kills it (reference).
One common agricultural use is boosting the growth of seedless grapes as the seed is an important site of gibberellin production for maturing fruits.
This pdf gives you a reasonable overview of what gibberellins do

Your reference link seems to be broken unfortunately.

@skymningen both links seem to be working for me. One of them is a pdf though, is that the one with the issue?

No, the reference was not working, now it is. Probably got edited.


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Is it a valid generalization that kinases catalyse reactions involving energy transfer and utilization?
The Wikipedia entry for kinase states that "a kinase is an enzyme that catalyzes the transfer of phosphate groups from high-energy, phosphate-donating molecules [such as ATP] to specific substrates".
ATP is the energy currency of the cell, so, would it be accurate to say that a kinase catlayses reactions involving energy transfer and utilization within a cell?

I intuitively think of kinases as switches: they allow molecules to exist as either a or b, and one or both forms may be active.

Care to elaborate, maybe with an example or two?

@CMosychuk — please follow the instructions for comments and do not use them to answer questions. It breaks the SE model and encourages others to do likewise.

Does the Wikipedia page on kinases not answer your question? Can you expand on what actually is the doubt, since the Wiki page has examples with specific functions fulfilled by kinases.

I have put in a quotation from Wikipedia (Google is not a source) for kinase, and modified your definition of ATP to make it more acceptable. Kinase is the name of a a class of enzymes that catalyse certain types of reactions. I assume you are familiar with enzymes. I am not sure, however, how one thinks "intuitively" about them. One can generalize about the sort of reaction they catalyse. Is that what you are asking?

@David I think the OP's meaning is best described in the last sentence. OP knows that ATP is a form of energy, and knows that kinases convert ATP to ADP while they transfer a phosphate group to another molecule. OP wants to know, then: is it correct to think about a kinase as an enzyme that delivers stored energy within a cell? In my opinion, a good answer would explain that OP's description sounds a little more like what many ATPases do: they are using the energy from ATP to do some energetically unfavorable work. But also explaining that kinases have different functions...

...and that in some anabolic pathways, yes, kinases are helping to deliver stored energy in the form of phosphate groups onto 'building blocks' of other molecules. But when a kinase adds a phosphate to regulate the function of another molecule, I wouldn't really say that it is delivering energy, just that there is some energy cost to doing the business of flipping cellular light switches, and ATP is readily available as a source to do that.

@BryanKrause That sounds like an answer to me.

Wanted to add, it is Phosphoryl group that it is transferring and not Phosphate. Wikipedia is not a very good source for learning.

@Tytoalba Good point, although I'd add that many sources besides Wikipedia talk about "transfering a phosphate" as the outcome of phosphorylation (I paged through some google scholar results for search terms like "kinase phosphorylation review" and confirmed this). I think it's intended as a bit of a shorthand, because the outcome is a phosphate group on the target, but it could also be a misstatement. For the biology (besides the specifics of the biochemistry) it doesn't really matter.

@Tytoalba Also I mostly blame the chemists who decided a phosphate+phosphoryl group would be called a "diphosphate", etc. ;)

I prefer the other term Pyrophosphate. @BryanKrause Yes it is Anidosinediphosphate again.

@Tytoalba I am familiar with the existence of the term "pyrophosphate" but I have never seen it used in a biological context or to name a biological molecule. This question from chemistry suggests that the "bisphosphate" terminology is becoming more common in biochemistry for ortho-phosphates, whereas "pyrophosphate" is really only used for the inorganic anion. However I don't expect "ADP" and "ATP" to change for quite some time, if ever. Alas.

I have rewritten the question to make it generally more useful (before I answer it). It is best not to have subjective titles — in general we are not interested in you particularly — and a statement that talks about an enzyme ”metabolizing energy“ clearly will not do. Even though you can talk about energy metabolism, this actually means the metabolic reactions in which molecules with the potential to transfer free energy are generated. This may seem high-handed, but SE encourages improvement of both questions and answers.

No.

It is not possible to suggest a verbal or pictorial generalization of
the role of kinases.
It is futile to try to do so as it is incorrect to think that
kinases have a single general role of the type suggested, or that the
utilization of free energy from ATP is limited to reactions catalysed
by kinases.

Clarification
Kinase is a surviving trivial name for enzymes that have been classified by IUBMB as ATP phosophotransferases. The categorization solely reflects aspects the chemistry of the reaction catalysed, and the sub-categorization in terms of substrate relects a diversity of roles. Moreover such kinase reactions are only one way in which the free energy of hydrolysis of the phosopho-diester bond of ATP can be utilized — transfer of the phosphoryl group to another molecule. Other types of reaction (and enzyme) are just as, if not more, important.
The diversity of roles played by kinases
I list at random some examples of different types of kinase reactions:

Hexokinase transfers phosphate from ATP to glucose. One purpose is
to creaate a charged molecule, glucose 6-phosphate, that cannot
go back across the cell membrane.
Thymidine kinase converts thymidine to TMP. Like several other
    kinases it can be thought of as catalysing a synthetic reaction, the
    phosphate being a part of the structure of the TMP (and ultimately
    TPP) molecules.
Protein kinases transfer phosphate to serine, threonine or tyrosine
residues of proteins. This is not using ATP for an energetic process,
but to cause a change in the structure of the target protein that
modulates its activity.
Creatine kinase interconverts creatine and ATP with creatine
phosphate (a rapidly mobilizable energy store in muscle) and ADP. As
the reaction is reversible it can be thought as either catalysing
the formation of creatine phosphate or its mobilization.
Pyruvate kinase is a similar to 4 in that it produces ATP, and as the reaction it catalyses is essentially irreversible in the cell, the name is quite
misleading about its function.

Non-kinase enzymes involved in utilizing ATP
These include ATPases, as @BryanKrause remarks, but also some others. Again, some examples at random:

Sodium /Potassium ATPase catalyses active cation transport.
Firefly luciferase (an oxidase) hydroyses ATP to produce light.
Glutamine sythetase (glutamate-ammonia ligase) uses the free-energy
of hydrolysis of ATP to convert glutamate and ammonia to
glutamine.

Your (original) description:

a kinase helps chemically deliver or metabolize stored energy within a cell

sounds a little more like what many ATPases do: they are using the energy from ATP to do some energetically unfavorable work, such as moving molecules or ions against their concentration gradients. However, kinases have a broad range of different functions.
In some anabolic pathways, yes, kinases are helping to deliver stored energy in the form of phosphate groups onto 'building blocks' of other molecules, and this stored energy can be used for future reactions.
However, when a kinase phosphorylates another molecule (often a protein) to regulate its function, I wouldn't really say that it is delivering energy, just that there is some energy cost to doing the business of flipping cellular light switches, and ATP is readily available as a source to do that. One big advantage of using kinases in these sorts of reactions is that, because a fairly large energy input is required, such reactions don't occur easily by mistake or just due to thermal energy.


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How to convert bwa mem output to BAM format without saving SAM file
I want to go straight from bwa mem alignment to BAM format as I don't need the SAM file and it takes up too much space. How do I achieve this?

For directly outputting a sorted bam file you can use the following:
bwa mem genome.fa reads.fastq | samtools sort -o output.bam -

Optionally using multiple threads:
bwa mem -t 8 genome.fa reads.fastq | samtools sort -@8 -o output.bam -

Ah, great solution if sorting is needed! I had tried this in the past but I was trying to pipe it though samtools view and then into sort. Didn't realise you could go straight into sort.

Found the solution. You just need to pipe the output from bwa mem into samtools view like so
bwa mem ref.fa in.fq | samtools view -bS - > out.bam

The - in samtools view tells it to read from stdin.

In my workflow, BWA output goes to MergeBamAlignment, so samtools view seemed lower overhead than samtools sort.  (Directly piping from BWA to MergeBamAlignment, as suggested here, failed for me.)


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What are the pros & cons of site-directed mutagenesis? What are the alternatives?
For a lab course we have been assigned to "remove a stop codon, using mutagenesis, that is in the middle of a gene in order for the full gene to be expressed. This will then fluoresce."
To do this we are considering site directed mutagenesis, which can replace the stop codon, however is this a good method? Are there any alternatives to SDM using Quikchange that are better? What are the pros and cons of the SDM we are thinking of performing? To see if we succeeded we will then use DNA sequencing and gel electrophoresis.
Our overall plan looks like this:

Gathering plasmids from E. coli
Gel electrophoresis of the plasmid DNA
Perform the mutagenesis using Quikchange
Transformation by heat-shock
PCR
Use a lac promoter to produce the gene protein

One issue I could think of was, how do we make sure the primers carrying the mutation don't anneal to each other due to their complementarity?
Is overlap-extension a good alternative? Are there any advantages to using transposon-based or point-directed mutagenesis?
Thank you!

If it were my lab, we'd just order a synthetic gene…

Depends... is this about the process or the result?

SDM will be the perfect tool for this mission, unless the plasmid in question is very large (20+ kb).
When you have performed the SDM, digest the products with dpnI to remove the original plasmids, transform e.coli and use a selective media matching your plasmid. Only bacteria with the plasmid will then be able to survive and form colonies, pick several colonies and perform a miniprep for each and sequence the area of interest. You can use the rest of the miniprep with the correct plasmid for transformation and expression. So skip step 5.

Although, as you say SDM is the most suitable tool, are the other forms of mutagenesis: transposon-based and point directed also applicable for this lab if we wanted to? And can you think of any cons with using SDM in this case?

The 'Quickchange' method is probably what you want. If you are worried about self complementary (which you shouldn't be too much) you can actually stagger the primers so they are not fully complementary. only the 10bp need to overlap where the mutation is. I included a small diagram below where the X marks the base you want to change

One alternative, which I use more than the SDM is by using TypeIIS restriction enzymes. This way you can mutate as many bases as you want in one go!
See this article


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From which animal is this derived?
I know only that it is not a bird and an insect. I am really interested in from what it is.

It looks like it could be some sort of internal cartilage, do you know anything more of its origin (where/when it was found, where was the picture taken, in what context...), i.e. could it be a sea creature for example?

Yeah it could be a sea creature.

Sorry it is a sea creature but it isn't a fish.

Please crop your image and specify the origin of the object.

That's the gladius (also known as pen) of a cephalopod, probably a squid. The gladius is an internal remnant of the originally external shell of cephalopods.
According to University of California Museum of Paleontology:

Members of the Coleoidea are probably the best known of the Cephalopoda, as this group contains the squids (Teuthoidea) and octopuses (Octopoda) [...] The majority of coleoids are squid species, and most of these animals are torpedo-shaped, fast moving, and have a thin, flexible internal shell called a pen.

And according to the Tree of Life project:

Other cephalopods have other types of shell remnants. The gladius lies within a sac, the shell sac, which secretes it and to which various muscles attach. The gladius has a variety of shapes and thicknesses, is composed mostly of chitin and is located in the dorsal midline and generally extends the full length of the mantle.

Here is one similar to yours:

Sources:

http://www.ucmp.berkeley.edu/taxa/inverts/mollusca/cephalopoda.php
http://tolweb.org/accessory/Cephalopod_Gladius_Terminology?acc_id=1955

What's its function?

@Tytoalba It supports some squid's muscles and helps swimming.

I concur with the answer of Gerardo Furtado. I sometimes go fishing and this looks exactly like the gladius (Fig. 1) of a loligo vulgaris (Fig. 2). The gladius is a hard internal structure in cephalodopds. In French we call that a "plume", as it has the appearance of a feather.

Fig. 1. The gladius, or squid pen. source: Oceans of Kansas

Fig. 2. loligo vulgaris. source: wikipedia


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How does the immune system fight scabies mites?
After a distressing episode involving my elderly mother and a nursing home, I've been reading up on scabies. It seems that in healthy people, the immune system limits the mite population to around 10 of the creatures at any one time; elderly and immunocompromised people can be infested by many more - thousands, even millions of mites (shudder).
So my question is, given that the mites burrow in the top, dead, layer of the skin, how does the immune system detect them and suppress them at all?
Conversely, if the immune system can limit the mite population so effectively, why doesn't it wipe them out entirely?

Welcome to Biology.SE! I think this is a very good question and made some edits to clarify it. Please feel free to further edit!

@Alex Thanks. I have only reverted the 'S' in the question, b/c I believe 'scabies' isn't a plural - same as eg 'measles'

Did you do any reaearch, say, into the immunology of susceptibility and resistance to scabies? If so, what did you find? On this site, some attempt to answer the question, even if the research doesn't help, is expected and appreciated. (Btw, I never heard that number. And from the numbers of healthy people I've had to treat for scabies - and having suffered a bad infection myself in early adolescence [an unforgettible experience] - I'd say the immune system is not all that great at suppressing the infection.)

@anongoodnurse  As in my OP, my research consisted of googling 'scabies', the results of which led me to those figures. (eg Wikipedia suggests a number as high as 2 million mites for encrusted scabies.)  I don't really have access to anything more specialised, which is why I posed the question on here.

while it seems that you're getting answers here, it's likely that SE Medical Sciences is a more appropriate forum for this question.

Found from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535073/
In addition to being a physical barrier, the skin is an immunological barrier63. The skin immune response is vital in wounding and infection and also modulates the commensal microbiota that colonizes the skin. Keratinocytes continuously sample the microbiota colonizing the skin surface through pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), mannose receptors and the NOD-like receptors. These receptors recognize pathogen-associated molecular patterns (PAMPs) including flagellin and nucleic acids, as well as lipopolysaccharide from Gram-negative bacteria, mannan and zymosin from fungal cell walls, and peptidoglycan and lipoteichoic acid from Gram-positive bacteria. The activation of keratinocyte PRRs by PAMPs immediately initiates the innate immune response, resulting in the secretion of antimicrobial peptides (AMPs), cytokines and chemokines. Beyond effecting an adaptive immune response, AMPs also directly kill bacteria, fungi and enveloped viruses64. Therefore, there is a constant interplay among keratinocytes, immune cells and microorganisms that is modulated by AMPs, cytokines, chemokines and microbial peptides.
While mites certainly are not fungal, viral, or bacterial, you can extrapolate the mechanisms required to prevent mite infestation being similar to those referenced above. Hope this helps!

This is an excellent question. We mostly hear about parasites being attacked by white blood cells, but mites are obviously too large to be phagocytosed, and furthermore the white blood cells are in the mite's stomach by the time they come into contact with the mite. Yet, mites are usually too small for us to see, so we can't crush them like we crush fleas. I know that aphids are eaten by other insects, but they are macroscopic, and I don't have any macroscopic insects on my skin. At the same time, when people get sick they start to be at risk for mite infestations. Also, sometimes one individual who is asymptomatic will give a mite infection to another individual, through close contact, which then causes a visible immune reaction in the victim: small red bumps indicating the locations of bites. This suggests that the immune system might be involved.
One theory is that we are looking for something like a mobile bacterium, which could live inside human white blood cells. Normally the bacterium would be dormant, but when white blood cells are ingested by a flea or a mite, the bacterium would start reproducing and releasing chemicals to counteract digestion by the parasite. Eventually the bacterium, if clever enough, would release enough chemicals to kill the mite that ingested it. However, mites have short lifespans and therefore evolve much more quickly than humans do. Unless your body can upgrade its defenses at the same pace, it will fall behind and mites will evolve resistance to the bacteria and its chemicals. The bacteria could evolve within the body, but we have no way to measure their fitness until after they are swallowed by the mite. So how could your immune system keep track of which bacteria are still effective against your mites? How does it know which bacteria should multiply and be deployed against future mites, and which ones are no longer useful?
From an information theoretic standpoint, in order for coevolution to occur, there needs to be some way for the bacterium to get back to the original host after living inside the mite. One way to accomplish this is if the bacteria kill mites by crawling up their throats and blocking them. Then when the mites try to feed a second time, some of the bacteria will get regurgitated back into the blood of the host, where it could be scavenged and returned to the lymph nodes for selection and review by the immune system.
Such a bacterium exists. Let's give it an alias: Bacterium X. Bacterium X blocks the throats of many kinds of fleas, as is well known. It can live inside white blood cells, usually being dormant in lymph nodes. Mites are observed to feed poorly on mice that are infected with Bacterium X, although they feed well on healthy mice. Fleas can transmit Bacterium X to new hosts both before and after they become blocked. Blockage in susceptible fleas leads to death by starvation. The bacteria is endemic in rodents worldwide, and normally harmless. However, when a pandemic strain emerges then it can be exceptionally virulent, producing lethal bacteremia in both human and rodent hosts. The Bacterium X disease condition is often characterized by swelling of the lymph nodes where the bacterium resides. Presumably, some of the high infectivity of pathogenic strains of Bacterium X could be due to its role as an endosymbiont, and the immune system's consequent eagerness to scavenge it from the environment so that co-evolution may happen.
The relationship of Bacterium X with mites is not well studied, perhaps partly because mites haven't been observed to transmit it between rodents, as fleas do. But many of X's traits in mites could be expected to generalize from its behavior in fleas; for example, smaller-sized species of flea are more susceptible to blockage, suggesting that mites, which are smaller than fleas, should be even more vulnerable to attack by Bacterium X.
I haven't given the actual name of Bacterium X because I wanted others to have the chance to figure it out. However, it is known that human white blood cells can contain multiple species of bacteria capable of killing fleas, in addition to the particular one I described. For me, an interesting question here is whether these bacteria are doing this on purpose, and if so, how the body keeps them evolving so that it can win the biological arms race against mites. However, I have trouble finding actual discussion of these ideas in the scientific literature. It seems possible that we have a tendency to want to view inter-species interactions as primarily hostile or pathological rather than potentially cooperative. Perhaps there is some other reason why evidences of symbiosis seems to go unremarked-upon, even when they seem fairly apparent: an ability for a bacterium to reproduce inside human and rodent macrophages, for example, or to kill a common insect parasite...

"mites are usually too small for us to see, so we can't crush them like we crush fleas."
Ah, you raise an interesting point - has anyone really tried ? I had scabies once, it was truly horrid and I scratched till I bled, which didn't stop the itching. Problem is that dead mites are just as provocative to the immune system as live ones. But I wonder if you could kill them by skin pressure before they proliferate ? I think they are probably evolved to survive pressure, but who knows ?

@JimmyWiddle Thanks for sharing. Yeah, if mites are anything like fleas ... fleas are almost indestructible. You said "I scratched till I bled" - maybe that is another way to encourage contact between skin parasites and the immune system. Mother always said "don't scratch, that will only make it worse", but I suspected this of being bad advice.


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What do we call this adjustable platform used to ensure that something is positioned strictly level in a lab?

This is an adjustable platform. Such a platform is used, for example, to make sure that a gel electrophoresis cassette is level relative to the earth. A passage in a procedure description which I'm translating says that the gel caster (the two glass plates between which we will pour the solution) should be put on top of this platform, after which the platform is adjusted "using a level". The text describes a vertical SDS-PAGE procedure.
I wonder what such benchtop lab platforms are called. In my Russian text it is called "заливочный столик" (pouring table, casting table).

I have never in my 5+ years in academic labs seen anyone use an adjustable platform for leveling... In general all tables in a lab should be level checked at installation so using such a platform would be overkill.

I remember using those for agarose gels as an undergraduate, though using them for PAGE doesn't make a lot of sense unless your bench is seriously out of level. Anyways, they can be called levelling tables and are used to promote uniform migration across the gel. Casting table also seems reasonable.


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Is the CMV promoter active in yeast?
I wish to transfect yeast and want to control my efficiency. So I thought to use pEGFP-N1 as control. The EGFP is driven by a CMV promoter. Can yeast read CMV promoters.
Thanks
Hermann

Yes (reference)
While I found your question interesting this was pretty much the first hit when I typed "CMV yeast" in google scholar. You should really look there first before you ask!