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Does a full tear of the gluteus minimus tendon has any functional implications?
From what I read on Wikipedia, all functions of the gluteus minimus are mirrored by the gluteus medius. Additionally, the gluteus medius is larger than the gluteus minimus (see comparative images here), which leads me to believe that the gluteus medius is stronger than the gluteus minimus.
Subsequently, I would tend to guess that a full tear of the gluteus minimus tendon does not have any functional implications. I.e., a human might have a full tear of the gluteus minimus tendon without any limitation of their movements. Is my guess correct?

You’re correct that the gluteus minimus is redundant in function with the gluteus medius, but an isolated gluteus minimus tear still causes functional problems because of the associated inflammatory response and subsequent pain deemed “greater trochanteric pain syndrome,” as the greater trochanter is the insertion site for hip abductor muscles like the gluteus minimus and medius:

MRI Web Clinic — May 2004,
  Gluteus Minimus Tear & Trochanteric Bursitis,
  Michael E. Stadnick, M.D. (mirror)

Clinical History: 70 year-old female with chronic left hip pain...What is your diagnosis?
Diagnosis: Gluteus minimus tear of the left hip with associated trochanteric bursitis.
Discussion: Lateral hip pain is frequently a challenging diagnostic and therapeutic problem. In the past, the presentation of chronic lateral hip pain with tenderness over the greater trochanter was attributed to trochanteric bursitis. This symptom complex, called greater trochanteric pain syndrome (GTPS), can mimic other serious causes of hip pain...Abductor tendon (gluteus minimus and gluteus medius) tears are becoming increasingly recognized as a frequent cause of pain at the hip. In fact, tears of the abductor tendons, instead of trochanteric bursitis, are likely the most common cause of GTPS.
In a large majority of patients, trochanteric bursitis or distension will accompany an abductor tendon tear. The frequent coexistence of trochanteric bursitis and abductor tendinopathy has led some authors to suggest that bursitis may in fact be a result of the underlying tendinopathy.
Early descriptions of abductor tendon tears at the hip emphasized involvement of the gluteus medius tendon as being most common. However, subsequent papers have revealed a roughly equal frequency of involvement of the gluteus minimus and medius tendons.

Thanks! Follow-up question: Does a full tear of the gluteus minimus tendon result in a long-lasting inflammatory response?


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Why does cholesterol need to attach to proteins to travel through the blood?
I guess the deeper question is: what makes it possible for proteins like those part of HDL and LDL to move through the bloodstream?

Ah, got it, thanks! With deeper question I meant: How do the proteins in LDL and HDL know that they have to go to the liver? How does their "GPS" work?

Maybe change the question - It think "Is there so called free cholesterol that travels through the blood?" should be some valid question, too, and sounds the same.

It is not LDL that does the Job. The target cells "know" which lipoproteins (LDL,HDL,VLDL...) they should take up. They express the specific Membrane receptor that binds the Protein part of e.g. LDL and therefore take up specifically LDL rather than e.g. HDL from the blood. Example: cells that express receptors for apolipoprotein B-100 (one of the Protein parts of LDL) specifically "filter" LDL from the blood. The "filtering" occurs via endocytosis. Hope that helps.

Thanks! So I guess LDL and HDL just moves through the whole circulatory system until it randomly hits the target cells.

In respect of "randomly hits..." the target might be at the other ending: how does LDL/HDL find the cholesterol. It does, and this refers to cholesterol being soluble in blood (maybe not soluble enough not to take the taxi..., some idea of mine). From Wikipedia: "ABCA1 mediates the efflux of cholesterol and phospholipids to lipid-poor apolipoproteins (apoA1 and apoE) (reverse cholesterol transport), which then form nascent high-density lipoproteins (HDL)." I do believe cholesterol not even esterfied is being shedded from cell for "random" uptake.

source: Stack Exchange

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

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What are the differences between insects and spiders?
I have always been told that a spider is not an insect, since the former has 8 legs and the latter 6 legs.
Is it just a matter of definition and spiders could have been defined as "8-legged insects"? Or are there more fundamental differences between the two kinds of animals and the distinction makes sense from the viewpoint of biology and evolution?

Spiders and Insects have been separate independent linages of animals for 500 million years. Spiders have two body parts (cephalothorax and abdomen), while insects have 3 (head, thorax and abdomen). Besides the differences in number of legs, spiders and insects have different forms of respiration, different mouthparts, and different exoskeletons. Insects have antennae, while spiders don't. In short, spiders and insects are more different from one another than mice are from sharks.

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


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What exactly does 'reverse use-dependence' mean?
I understand 'use-dependence' related to a drug, for instance, more angiotensin2 effects in a hypertensive more prominent is the action of angiotensin2 receptor blockers. But I do not get the term, 'Reverse use-dependence'.
https://en.m.wikipedia.org/wiki/Potassium_channel_blocker
In this site, in Medical Uses, the term is mentioned.

Reverse use dependence is the reduction of a drug's efficacy with the repeated use of the target. This contrasts with ordinary use dependence, for instance with $\mathrm{Na}^+$ blocking local anaesthetics, where they exert more block after tissue use. Reverse use dependence is particularly (but not exclusively) seen with channel blockers such as quinidine.
Quinidine is a $\mathrm{Na}^+/\mathrm{K}^+$ blocker that can slow heart rates, and does so more effectively when the heart rate is already slow. Increased use of the tissue, with a raised heart rate, reduces the effectiveness of the drug. So, strangely, quinidine exerts less block when the target is in use. This is shown in figure 4 from (Breithardt et al., 1995). As the tissue is used less (cardiac cycle length increases), the effect of the drug becomes stronger (action potential duration prolongation increases).

The reverse use dependence of quinidine can be demonstrated on a molecular level with application of quinidine to a voltage-clamped channel with an $\mathrm{i}_\mathrm{Ks}$ current. We see better block when short electrical pulses are given than when longer ones are. The mechanism behind use- and reverse use dependence is by state-dependent affinities, e.g. the drug can bind more easily to the channel in open/closed state. For example, a channel blocker whose binding site becomes occluded when the channel is opened could exhibit use dependent block.
But be warned: reverse use dependent drugs may also exhibit normal use dependence. Quinidine is not just reverse use dependent, but also use dependent
as a $\mathrm{Na}^+$ blocker. The type of tissue and its state change the effect of the drug and must be taken into account.
See (Breithardt et al., 1995) for a review of the topic:

In 1990 Hondeghem and Snyders introduced the concept of reverse use dependence as being a drug effect which is less marked with increased use. Specifically
  quinidine, N-acetyl-procainamide and sotalol lengthened action potential
  duration markedly at slow heart rates but much less or not at all at fast heart rates
  (Fig. 4 [27)). Frequently, reverse use dependence has become equated with reverse
  use-dependent block of ion channels. Although reverse use-dependent block of ion
  channels can lead to a reverse use-dependent drug effect, this does not need to be
  the case. Worse, reverse use-dependent drug effect does not require reverse use dependent block of channels.

References:

Breithardt, G., Borggrefe, M., Camm, A., Shenasa, M., Haverkamp, W. and Hindricks, G. (1995). Antiarrhythmic Drugs. pp.97-98.


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Is there a scientific explanation for male and female fragrance preferences?
The following is only anecdotal evidence, but in my experience it's very consistent.
When products have added fragrance (cosmetics, soap, air freshner, candles, etc), women often seem to enjoy the fragrance whereas men's reaction is normally something from indifference to outright revulsion.
I've tried googling this but the results are all about sexual attraction, which I'm not asking about.
One could speculate that this pattern is because the folks in marketing have worked out that adding fragrances will make women buy things and that as far as men are put off by fragrances, that doesn't have a net negative sales impact. But such theories don't answer the underlying question:
Why is there a difference in experience between men and women reacting to the same fragrances in the first place? Is there a "hard science" explanation for this phenomenon?

Are you sure this isn't individual or cultural, rather than biological?  I'm male, and while I don't use many products with added fragrance, I do fill my garden with fragrant plants.

I am a woman and I also find most of added fragrances revulting. Among the small set of my female friends it seems they usually try many different products before finding the one with smell they like. Our personal tastes are mostly incompatible between each other. I haven't seen my male friends spending time to try and sniff multiple products in order to select the preferable ones. I have seen some go for the first one fitting all requirements as written on bottle without even sniffing it once before buy.

The idea that males and females react differentially to various smells in the context of “hard science” alludes to the concept of sexual dimorphism in olfactory signaling, which has been investigated:

Stowers & Logan. Sexual dimorphism in olfactory signaling. Current Opinion in Neurobiology. 2010. 20,770-775.

What makes males and females behave differently? Although genetic master-regulators commonly underlie physical differences, sexually dimorphic behavior is additionally influenced by sensory input such as olfactory cues. Olfaction requires both ligands for signaling and sensory neural circuits for detection. Specialized subsets of each interact to generate gender-dimorphic behavior. It has long been accepted that males and females emit sex-specific odor compounds that function as pheromones to promote stereotypic behavior. Significant advances have now been made in purifying and isolating several of these sex-specific olfactory ligands. In contrast, the neural mechanisms that enable a gender- dimorphic response to these odors remain largely unknown. However, first progress has been made in identifying components of sexually dimorphic olfactory circuits in both Drosophila and the mouse.

You’re right that most research in humans (like this paper) on this subject includes elements relating to sexual orientation or sexual selection, but I did find one article that is more relevant to your question:

Lindqvist. Preference and Gender Associations of Perfumes Applied on Human Skin. Journal of Sensory Studies. 2012. 27,490-497.

Abstract

The perception of fragrances has been a growing field of interest, where perfumes classified as either typically feminine or typically masculine primarily have been used as stimuli. The current study explored gender associations and preferences of more “unisex” perfumes found in the middle of a gender continuum of fragrances, both when the fragrances were applied on humans, and when they were presented in glass bottles. Blindfolded participants indicated if they wanted to use the fragrances themselves, if they wanted their partner to use the perfumes, scaled gender associations (femininity and masculinity) for each perfume and tried to guess the gender of the person each perfume was applied on when not presented in a bottle. Results show that the gender of the person that the perfume was applied on did not affect the participants' preference or their gender scaling. Moreover, the preference did not differ between female and male participants, indicating that the commercial gender categorization is less important to the perfume consumers.

Practical Implications

On the commercial market, most perfumes are classified as either feminine or masculine, although the odor quality of feminine and masculine odors are overlapping and constitute a continuum rather than two separate clusters of odors. Earlier research has shown that participants tend to prefer perfumes positioned in the middle of this gender continuum. The current study investigates gender associations and preferences of perfumes from the middle of the gender continuum while these are applied on humans. When blindfolded participants evaluated their perception of the perfumes in this study, it became clear that neither the gender of the humans that the perfumes were applied on, nor the commercial gender labeling of the perfumes were important to their perception. Consequently, the commercial gender categorization does not seem to be sufficient for all perfumes. Instead, the classification of perfumes could be according to other aspects, e.g., according to odor quality.


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How valid is Schwartz's criticism of molecular phylogenetics?
A proponent of the human-orangutan clade, Jeffrey Schwartz argues, in this paper [1], that molecular phylogenetics is largely based on a baseless assumption.
To sum up, according to him:

this type of phylogenetics relies on overall similarity, rather than cladistic considerations, to infer relationships. He claims that even parsimony algorithms (albeit traditionally contrasted with distance-based methods) group taxa on the basis of overall similarity.
this reliance on overall similarity is based on the baseless and questionable assumption that sequence evolution is gradual and continuous.

Could you tell me if his objections and paper hold water, and how valid they are?
[1] Schwartz & Maresca, 2006, "Do Molecular Clocks Run at All? A Critique of Molecular Systematics", Biological Theory, Springer.

Heaven preserve us from phylogenetic flame wars! As was said by Lord Palmerston about the Schleswig-Holstein question, only three people understand it, the Prince Consort who is dead, a German professor who has gone mad, and he himself who had forgotten all about it. I don’t fancy your chances of resolving it here.


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What is this fruit
What is this fruit? Is it edible?
Found it in my backyard, in the Lehigh valley, eastern PA.
Here's the photo:

Is a better photo possible? Maybe a photo of the entire plant with leaves?

What is the size of the fruit? Did you find any more? What habitat did you find it in? Can you describe or provide a photo of the plant it came from? Did you cut the fruit open - if so, please describe or provide a photo. Species ID questions need to be detailed and complete to avoid getting wrong answers (especially those that are unfortunately upvoted due partially to question vagueness). Please [edit] your post with more details to ensure you get an accurate answer. Thanks.

Considering how many of them I’ve seen growing on the ground where I live in PA, it’s likely a mock strawberry. The plants grow on runners on the ground and have yellow flowers with five petals that become the fruit. The seeds come off easily when you rub it.
They’re safe to eat (wash them and make sure your lawn isn’t treated with chemicals though) but lack the flavor of real strawberries. I’ve eaten them before.
The fruit doesn't get much bigger than the one you're holding either. Here is a zoomed-in picture from Wikipedia:

Please provide a direct citation regarding the safety of eating the species you list. You must realize you're encouraging someone to eat a specimen you've ID'd from a poor-quality photo and without documenting that you've done your own homework on the safety of doing so. Personal experience is valuable but not good enough to suggest that someone else try it. (this is especially true for a fruit that's historically been regarded as dangerous to eat). Please [edit] your post to provide stronger evidence for the safety of consuming this fruit or please remove the statement about its consumption.

A reputable citation such as this would be preferable.

@theforestecologist Technically I cited Wikipedia which cited that page, but now I’ve linked to it directly.

thanks for the edit. Suggesting that something is safe to eat to complete strangers likely should be supported more directly than a footnote in a link. (FYI I've seen someone try to eat an Amanita mushroom before based on incomplete/faulty (and not at all cited) information.) In this false-strawberry case it doesn't appear to be all that big a deal, but it's just good practice when sharing information online. More generally, we prefer that all major claims made in posts on Biology.SE be supported directly. Thanks :).

It looks quite similar to the fruit of arbutus unedo (a.k.a. strawberry tree), which is edible:

But your image is too low definition to be certain.

-1. Thanks for the answer but this is almost certainly WRONG. This shrub is found in the  Mediterranean region of Europe, not Eastern Pennsylvania (USA). According to your Wiki article, the plant is found in the US, but it has been planted in the mediterranean climate of Western USA -- again, quite a different climate than Pennsylvania. Also note that the fruit of your tree grows to be larger than the specimen in the OP's picture.


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Does a full tear of the gluteus minimus tendon result in a long-lasting inflammatory response?
Does a full tear of the gluteus minimus tendon result in a long-lasting inflammatory response?
This answer mentions:

An isolated gluteus minimus tear still causes functional problems because of the associated inflammatory response

But I read on {1}:

“signs of either acute or chronic inflammation have not been found in any surgical pathologic specimens in patients with clinically diagnosed lateral tennis elbow syndrome,”

Note that tendon tears are present in a tennis elbow (a.k.a. lateral epicondylopathy). From {2}:

Review of MRI findings from 24 patients with epicondylitis reported increased intratendon signal on both T1 and T2 pulse sequences58 with occasional bone marrow edema pattern in the epicondyle. Other studies have shown thickening, edema, and tears of the common extensor tendon.

References:

{1} Bass, Evelyn. "Tendinopathy: why the difference between tendinitis and tendinosis matters." International journal of therapeutic massage & bodywork 5, no. 1 (2012): 14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312643/
{2} Taylor, Samuel A., and Jo A. Hannafin. "Evaluation and management of elbow tendinopathy." Sports Health 4, no. 5 (2012): 384-393.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435941/

Why are you comparing a non-tear injury (tennis elbow) to a full tear of a tendon (gluteus minimus)?

@CharlesE.Grant tennis elbow is micro tear

Micro-tear seems very different then a full tear.

@CharlesE.Grant I don't know whether the difference impact the inflammatory response

The article you linked is interesting, but as @Charles E. Grant mentioned in the comments, it’s not particularly reasonable to compare a non-tear repetitive stress injury (like epicondylitis) to a full muscle tear. Non-tear repetitive stress injuries persist because the offending frequent motion doesn’t stop. A muscle tear, however, will recruit an inflammatory response that will eventually be resolved by anti-inflammatory factors (Th2 cells directing the cellular microenvironment towards healing / scarring).
This healing process might not result in an optimal resolution of the initial injury, and it’s not unique to any particular body system. Rather, pretty much anything in your body that can be injured will first respond with a period of innate inflammation followed by fibrosis and resolution (whether or not that restores function / alleviates pain depends on a number of factors including injury severity, therapeutic management, and healing conditions e.g. if there were repeated injuries during the healing process).
With regard to gluteus minimus tears — it depends on the injury. If a patient persistently aggravates an already-torn muscle, they will have more inflammatory cells recruited to the injury. If they do a good job allowing the injury to heal (not re-aggravating the injury, receiving surgery if structural correction is required), the inflammatory process will resolve relatively quickly.

Thanks. As mentioned in my comment in reply to @Charles E. Grant, tendon tears are present in an epicondylopathy (and more generally, any tendinopathy resulting from  repetitive stress). I have added one reference supporting this statement in the question. I believe there is a consensus from the medical community on this.

I think your second reference essentially corroborates what I’ve written above: “Four stages of lateral epicondylitis have been described, beginning with the early inflammatory reaction, followed by angiofibroblastic degeneration, structural failure, and ultimately, fibrosis or calcification.”

That's correct, I agree with the rest of your answer. I'll add another follow-up question tomorrow.

Follow-up question: Can an individual further aggravate a full tear of the gluteus minimus tendon (trochanter insertion)? Your insights are welcome!


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What kind of shiny bronze beetle is this?

Lots of these on my rosemary bush
About 7mm long

Please provide your location. Thanks.

The plant helped identifying the beetle: This is a rosemary beetle (Chrysolina americana), which feeds on rosemary,  lavender and thyme. See here and here for some more information.


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What does this skull belong to?
I was cleaning out my pool with a leaf scoop the other day and found a small object, which I assume to be a sort of skull or cartilaginous structure of something that had died.
I live in Sydney, Australia and in the pool there were a large quantity of water boatmen and dragonfly nymphs.
What does this skull belong to, and what is the purpose of the hollow, bulbous mounds next to the eye sockets?


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Is there any checked case of "involution"?
I know that strictly speaking the term "involution" referring to the evolution theory doesn't hold any meaning. Organisms keep on evolving and changing with time, that's all.
But the following situation could perfectly happen:
Some event causes some organisms to evolve certain characteristics that allow for a better survival, but with time that event stops and what was previously and advantage for these organisms, now it's a disadvantange, and to adapt to the new situation what they do is to exactly remove these characteristics and they end up being exactly the same as they were previously to the change. It could be considered that they have "involutioned".
Are there checked examples of this? (Not just as theory, examples of organisms where this "involution" has been observed). I'm specially interested in "complex" organisms, I think this is not that far fetched to happen to organisms like bacteria, virus or the like. But for more "complex" organisms I guess it's too much of a coincidence.
Edit: I'm putting an example to clarify:
Let's imagine we have a huge amount of plants of the same species which can grow extremely fast (in the way they could simulate 100000 years in evolution in one hour) and we have an atmosphere for them that is the same as current one. (Not realistic, but let's make the thought experiment). We also put some put of these plants apart.
Little by little we go changing all the carbon dioxide in that atmosphere with something, like, for example, nitrogen, it's to expect, that, with time, some plants will appear to better use the nitrogen, at least up to the point where they can survive, as carbon dioxide is every time lower and lower and plants not adapted to this end up dying.
When we finally have only nitrogen processing plants we start the opposite, we start filling little by little with carbon dioxide, it's to expect that the contrary would happen.
Now, if a biologist were to observe the plants that were set apart at the beginning and the new created plants he wouldn't be able to tell where each plant is from, unless he was aware they were separated to do the experiment.

Are you asking about an example of varying selection pressure (with associated adaptation) over time? Something like "temperature decreases, creature evolve to be more hairy. Temperature increase back, creature evolve to be less hairy"?

@Remi.b, it's more than that, it would be creature evolves to be more hairy, creature goes back to be the same.

Isn't it exactly what I suggested? I had never heard of the concept of "involution". According to wikipedia it refers to the physiological change in organ size. It has nothing to do with evolution. You might want to just get rid of this term alltogether and just ask for an evidence of varying selection pressure (with associated adaptation) over time? Eventually, add a specific example (such as my hairy/hairless example) with it for clarification.

"Involution" is basically a made up word that doesn't hold any meaning in this context, although it's translation is used in my native language for describing behaviors that people make that are not supposed to happen nowadays, as if it were to mean that they are some previous organism. But well, we can forget about the word and I'll put an example that clearly explains it.

Yes there are several examples of retrograde evolution (traits present in ancestors but lost in a species). It can be subtle as loss of some non-central metabolic pathway (Vit-C synthesis) or drastically visible as loss of body parts (for e.g. limbs of snakes). I just saw an entire book on this topic. But there can be drastic trait losses in micro-organisms too (for e.g. loss of mitochondria). Is this what you are looking for?

Australian kangaroos were originally rather small marsupials which evolved into megafauna due to a changing environment. We are not certain as to why the megafauna went extinct, though we do know that their size was reduced to what it was previously, albeit some alterations in skeletal structure and such had occurred.

"Exactly the same" probably doesn't fly, just because there is so much possible variation, but for a fairly obvious example, consider birds.  Their ancestors evolved flight: some modern-day birds (ostriches, emus, kiwis, &c) have lost that ability, though their vestigal wings haven't re-evolved into legs.  But consider the evolutionary link between birds and theropod dinosaurs, and how many of those (e.g. T. rex) had vestigal forelimbs.
Another example would be dolphins and ichthyosaurs, which both independently "involved" from land-dwelling creatures back to a form that's similar to the ancestral fish.
But of course neither of these are really "involution" in the sense of reversing an evolutionary path.  They are cases of organisms exploring new evolutionary paths, where the environmental pressures (such as need for streamlining to move efficiently in water) cause them to resemble some ancestral form.


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High-res / high quality, public domain cell / bacteria images on the web for download
Wondering if there are any high quality, high res images of eukaryotic cells or bacteria on the web available for download (public domain). I found some illustrations which are public domain, they look nice, but they are illustrations. I would like to find SEM electron micrograph images or things of that nature, microscope images in the public domain.
Here is an SEM image that is somewhat acceptable, though it has the legend built into the image and isn't colorized (colorization would be a bonus). Here is a colorized image.
This is more the quality I am looking for.
This is decent, but it's not public domain.
These are great!
I wish some of these were public domain.

What do you want to do with them? Is it commercial use as suggested by your attitude to a CC image? Nobody ca stop you downloading for private use unless they are watermarked.

I want to give them away and let others sell them

Then — and in any case — this doesn’t appear to be a question about biology in the terms of SE Biology, I’m afraid.


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What's up with this leaf?
This cool design was "tattooed" on this leaf.
I found it on the windshield of my car.
What's up with it?

That is the work of a leaf miner. A leaf miner is the larval stage of an insect that feeds on the inside layer of leaves. Notice how the galleries (tunnels) start small and then get larger as the larva matures? Most leaf miners are moth larvae (Lepidoptera)
https://en.wikipedia.org/wiki/Leaf_miner

I love this caption from the wiki page photo: "Leaf with minor miner damage".

@pyro Since the miner isn't an adult, you could even describe it as minor miner minor damage!

This leafminer is a moth in the genus Phyllocnistis (Gracillariidae). If you knew what plant the leaf came from, the moth could probably be identified to species. The marginal leaf fold at lower right is where the mature larva has spun its cocoon.
Incidentally, I'm just finishing a complete guide to the known leafminers of North America. There are many species left to be discovered though!


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Can a pathogen be totally resistant to the human immune system?
Can a pathogenic organism be totally resistant to the human immune system? For the purpose of this question, the organism in question must cause a disease.
Examples of organisms that would qualify as totally resistant:
Pathogenic organisms that are completely undetected by the immune system while the disease that they cause runs its course.
Pathogenic organisms that, even if detected, are completely invulnerable to the immune system. For instance, macrophages and other immune cells would not be able to destroy even one cell of such an organism.
Is it possible for such a pathogen to exist? Are there any such pathogens?
(For the purpose of this question, the HIV and diseases that only manifest in immuno-compromised individuals do not count)

The problem is  much of the immune system is passive, that is it resists everything equally.

???? The HIV attacks the immune system. The infection is obviously easier in already immuno-compromised individuals...

I can't think of any pathogenic organisms that are completely resistant to the immune system. Some bacteria that cause chronic diseases (e.g. tuberculosis) are relatively resistant, and a handful of viruses (e.g. spumaviruses) are relatively invisible, but the nature of pathogen transmission would mean that completely resistant organisms would spread through a population pretty fast and we'd know about it.
Pathogenic prion agents, like scrapie and Creutzfeld-Jacob disease, are essentially invisible to the immune system, and can be transmitted; but they aren't pathogenic organisms. They might be the closest to your description though.


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For each movement performed by both the gluteus minimus and medius, what percentage of the movement do the gluteus minimus and medius account for?
From what I read on Wikipedia, all functions of the gluteus minimus are mirrored by the gluteus medius. Additionally, the gluteus medius is larger than the gluteus minimus (see comparative images here), which leads me to believe that the gluteus medius is stronger than the gluteus minimus. I wonder to what extent it is stronger.
For each movement performed by both the gluteus minimus and the gluteus medius, what percentage of the movement do the gluteus minimus and the gluteus medius account for, respectively? (e.g., 80% of the strength stemmed from the gluteus medius, and 20% of the strength stemmed from the gluteus medius)


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Quick overview of how to capture microscope images of histology plate or fluorescent plate
I am looking at these two:

I would like to DIY take photographs of plant and animal cells using a cheap microscope such as this:

I don't know too much about microscopes or the techniques to do the staining, but that is what this question is about. I would like to know briefly what is required (tool-wise and material-wise) to capture images like the two above.
For fluorescent microscopy images, wondering if I actually need a fluorescent microscope, or if I can make do with a regular optical microscope. If I need a fluorescent one, wondering if there is anything else needed, like special lighting or special materials for tagging the cells, which seems like it might require extra stuff like centrifuge and who knows what else. In that case I would just like to get a sense for how complicated it is to do fluorescent microscopy.
For the histology slides, wondering generally what it takes to do that too, if I can get by with a regular microscope.
Generally wondering what equipment is required to accomplish these two images.
So far I have a DSLR camera and am imagining a basic optimal microscope with a DSLR adapter, and perhaps some basic dies that I would just drip into the slide (don't even need a pipette). That just shows my simplistic understanding, maybe fluorescent microscopy requires advanced biotechnology of some sort, which is sort of what I'm wondering, what the basics are.

For fluorescent microscopy images, wondering if I actually need a fluorescent microscope, or if I can make do with a regular optical microscope.

You need a fluorescence microscope. You need to be able to excite your sample with a narrow wavelength of light, and then image a different wavelength of light that is emitted. You need mirrors, emission and excitation light filters for that. You also need to understand the process. If you don't, having software to do the 'thinking for you' such as overlaying the different color channels is a nice thing, but then it's another requirement.

If I need a fluorescent one, wondering if there is anything else needed, like special lighting or special materials for tagging the cells, which seems like it might require extra stuff like centrifuge and who knows what else.

Samples can sometimes have autofluorescence (e.g. the chitin that makes up the cuticle of insects is autofluorescent) but most samples are not. Almost always a fluorophore is used to stain the specimen for something. These can be cheap or very expensive, depending on what you want to stain. This really depends on your sample and how it is prepared. And know that most 'good' samples' are dehydrated or are treated by chemical fixation, which requires chemicals you cannot usually find at a local pharmacy. It depends on how ambitious you want to get as an amateur microscopist!
Also, you won't need a centrifuge.

For the histology slides, wondering generally what it takes to do that too, if I can get by with a regular microscope.

You can get by with a regular upright widefield microscope for sure. If you perform the sectioning well (making thin slices of your sample) then even basic microscopes will produce fascinating images, provided your lighting is good. It helps to have a condenser or a nice lamp and some thin and clean glass slides for well illuminated images.

Maybe fluorescent microscopy requires advanced biotechnology of some
  sort, which is sort of what I'm wondering, what the basics are.

It requires a little bit more optical work. I would stay away from it unless you are serious, because it takes quite a bit more work and equipment to make it minimally workable. Normal microscopy is certainly a lifetime of fun if you have the desire to find interesting samples and work to make them good for imaging.
Addendum: the principle of fluorescence microscopy is quite simple but aligning everything is actually quite difficult if you are an amateur with no specialized tools. Here is the principle only, notice how the input and output must be aligned and the small objective lens has to transmit both excitation and reflected light:

And here is an example of a basic lab stain for two elements of the cytoskeleton (actin in red and microtubules in green) and a DAPI-type stain for nucleic acids (that shows you the DNA-rich nucleus in blue). The crispness of the image really depends on the use of at least two or three lasers (not epifluorescent illumination, i.e. "lamp nearby") to produce the necessary and specific narrow excitation to separately image the different channels. The light detectors are in black and white (for increased resolution), and only in post-processing are they color-coded to make the image pretty.

For a start I would begin with the basics! Pollen, cells on the inside of your cheek, blood, a single onion layer (...is a monolayer of cells, perfect for imaging), anything else you find and can think of! And find yourself a nice stain, or a nice dye or ink that is partially permeable. The world is your proverbial oyster at this point.


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Can anyone tell me what type of snake this is?
I found this snake in my garden and I'm wondering what type of snake it is! It was around 1 metre long and I'm in Lincolnshire UK.

It was around 1 metre long and I'm in Lincolnshire UK

With all due respect, it's fairly common knowledge that there are (essentially) only 4 native snakes in the UK: the adder, grass snake, smooth snake and barred grass snake. If you see a snake in the UK, chances are it's one of them.

I believe this is a Barred Grass Snake, Natrix helvetica. There are only a few snakes naturally found in the UK, and the Grass Snake matches the size, color, and pattern (bars on the sides but not on the back). The "N. helvetica" designation is relatively new, 2017, following genetic testing that showed that the previous name of Natrix natrix was not correct. "The newly distinguished snake is grey, not olive green like the N. natrix and does not have the same bright yellow collar."

Youtube video
Stock photo from Alarmy
Publication describing geographical distribution: Phylogeography and taxonomy of the barred grass snake (Natrix helvetica), with a discussion of the subspecies category in zoology. Figure 1 (below) includes a photo

Smooth Snake is another possibility but seems much less likely to me.

Smooth snakes are slender and normally grow to around 55 cm (2 ft). They are grey or grey-brown with darker markings along their back and usually a 'butterfly' shape on the top of their head. They are very rare in the UK but can be found in heathland habitats in Surrey. It would be very unusual to find a smooth snake in your garden. They are very secretive and would normally be found underneath objects.

--Which snake is it?
 (My emphasis)

Smooth Snake.
1 Metre long is a bit large for this species, but it is in that range and it is where you live.

Both sexes grow to an average length of about 60 cm (24 in) to 75 cm (30 in). Two specimens measuring 83 cm (33 in) have been recorded in Sweden, as well as one in Russia that was 92 cm (36 in).
[...]

 Smooth Snake - Wikipedia

Here is another picture of the snake, which seems almost identical to yours.


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Cooperative Enzyme Question
I'm currently studying for the MCATs. After doing some biochemistry practice questions, I came upon a question that I believe may be incorrectly posed. I was wondering if I'm correct in saying this or not.
The question is: " A certain cooperative enzyme has four subunits, two of which are bound to substrate. Which of the following statements can be made?"
The correct answer is "The affinity of the enzyme for the substrate is greater than with one substrate bound."
My confusion lies in the fact that the question never specified whether this cooperative enzyme had a positive or negative Hill coefficient. When approaching future questions like this, should I assume a positive Hill coefficient?

You need to rephrase your question. This list cannot give advice on interpreting examination questions, or whether questions are ambiguous. Only questions about biology are valid. We can answer questions about the binding of substrates to enzymes showing positive or negative cooperativity or whether such enzymes exist. These might be a way of establishing whether or not you are correct. Then you can draw your own conclusions about the academic level at which the question is pitched and your best examination strategy.


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Edible macroalgae?
I know that kelp is edible because the concept of eating kelp is all over the interwebs.  However, there is incredibly little information available online about what species of "seaweed" is edible.  I specifically am currently staying on Lake Geneva, and would be especially interested in edibility information about plants living in the lake, such as starry stonewort.  However, given the seeming general lack of information about the subject online, I would love to know about any common species of easily-accessible (e.g. by skin-diving) seaweeds that are edible and have any manner of nutritional value.
What species of seaweeds are edible?

this paper has a nice list of species found in Lake Geneva.  Most prominent are the Chara, Nitellopsis and Potamogeton genera.  Apparently Chara and Nitellopsis are common invasive species all over the place.  Information specifically regarding the edibility of these would be most valuable.

Edible (marine) seaweeds with nutrition facts:

Kelp: Kombu, Arame, Wakame
Red alge: Nori, Dulse, Irish moss, Laver
Hijiki

Other types of edible marine seaweed:

Red algae: Carrageen moss
Green algae: Sea lettuce
More edible seaweeds with pictures on Wikipedia on Food and Agriculture Organization

Freshwater macro algae are often toxic (Wikipedia, Biology Libre Texts). Starry stonewort does not appear to be edible, either.


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Blood acidity and bones
By consuming acidic foods, could one cause their blood to become acidic and therefore cause an acid+base reaction between their blood and bone?
I ask this because i recently discovered bone is a base, as its chemical formula is approximated as Ca10(PO4)6(OH)2 where the (OH)2 suggests bone is basic and thus prone to a neutralisation reaction with acidic blood. If so, what salt would be produced?

The answer to this question What are the highest and lowest possible pH, paCO2 and HCO3 in the blood of living human? offers normal ranges for blood pH. You can see that the range is very narrow and never becomes acidic. There is a great deal of nonsense written about blood pH and food, almost all of which is complete garbage and should be ignored.

i admit the nonsense you speak of was this question's inspiration haha

Short Answer: As the comments mention, this is a hot topic for pseudoscientists to use as a selling point for their supplements. There is limited evidence that dietary acid intake significantly alters bone resorption, especially in the setting of normal renal function. This paper should answer all of your questions (emphasis mine):

Frassetto, Banerjee, Powe, Sebastian. Acid Balance, Dietary Acid Load, and Bone Effects—A Controversial Subject. Nutrients. 2018. 10(4),517.

Abstract: Modern Western diets, with higher contents of animal compared to fruits and vegetable products, have a greater content of acid precursors vs. base precursors, which results in a net acid load to the body. To prevent inexorable accumulation of acid in the body and progressively increasing degrees of metabolic acidosis, the body has multiple systems to buffer and titrate acid, including bone which contains large quantities of alkaline salts of calcium. Both in vitro and in vivo studies in animals and humans suggest that bone base helps neutralize part of the dietary net acid load. This raises the question of whether decades of eating a high acid diet might contribute to the loss of bone mass in osteoporosis. If this idea is true, then additional alkali ingestion in the form of net base-producing foods or alkalinizing salts could potentially prevent this acid-related loss of bone. Presently, data exists that support both the proponents as well as the opponents of this hypothesis. Recent literature reviews have tended to support either one side or the other. Assuming that the data cited by both sides is correct, we suggest a way to reconcile the discordant findings. This overview will first discuss dietary acids and bases and the idea of changes in acid balance with increasing age, then review the evidence for and against the usefulness of alkali therapy as a treatment for osteoporosis, and finally suggest a way of reconciling these two opposing points of view.

This paper is open-access and I recommend you read it, but the conclusions summarize their findings nicely:

7. Synthesis

We suggest the way to put all of this information together is to agree...that bone alone cannot buffer the positive acid balance that one can calculate from measures of acid production and acid excretion. In addition, endogenous acid production goes up and down in an attempt to maintain systemic blood pH...
Diets high in acid precursors add to the body’s acid burden. For the majority of people eating typical western diets with acid loads of ≤1 mmol/kg, whose renal function and acid excretory ability is normal, dietary acid loads would not be a readily detectable factor in altering bone mineral density leading to the development of osteoporosis. Other factors such as age, gender, race, and immobility are quantitatively more major factors in determining bone mass and bone breakdown.
However, body retention of only 1 or 2 mEq of acid each day, barely detectable by current measurement techniques, buffered by muscle and kidney and titrated by skeletal base over decades, could potentially result in major depletion of bone mineral. Thus, we suggest that those older subjects with diminished renal function, decreased renal acid excretory ability, and lower buffering capacity due to lower muscle and/or bone mass, whose diets contain high net acid loads could potentially benefit the most from alkali therapies.

Long Answer: Although there's a wealth of pseudoscience on the internet relating to acidemia and bone composition, there is some truth to the idea that bone can be affected by pH. An excellent model to explore this concept is chronic kidney disease, as impaired renal function causes decreased H+ secretion, which results in a chronic metabolic acidosis:

Kopple, Kalantar-Zadeh, Mehrotra. Risks of chronic metabolic acidosis in patients with chronic kidney disease. Kidney International. 2005. 67(95),S21-27.

Metabolic Acidosis

Severe chronic metabolic acidosis (i.e., the presence of excess hydrogen ions in blood) has two well-recognized major systemic consequences. First, metabolic acidosis, or acidemia, induces increased protein catabolism, decreased protein synthesis, and negative nitrogen and total body protein balance, which improve upon bicarbonate supplementation. Second, metabolic acidosis causes physicochemical dissolution of bone and cell-mediated bone resorption (inhibition of osteoblast and stimulation of osteoclast function).

Metabolic Acidosis and Bone Disease

Metabolic acidosis exerts multiple effects on bone. It causes the physicochemical dissolution of bone and cell-mediated bone resorption through the inhibition of osteoblast activity and stimulation of osteoclast function. These events are associated with a loss of calcium and phosphorus from the bone. Metabolic acidosis stimulates osteoblasts to release prostaglandins. This stimulates osteoclast function and inhibits osteoblast activity. Glucocorticoids can inhibit the production of prostaglandins by osteoblasts.
Metabolic acidosis is also associated with a decrease in the content of bone bicarbonate. Additionally, bicarbonate supplementation in postmenopausal women is associated with decreases in urinary calcium, phosphorus, and increased osteocalcin levels, indicating a beneficial effect. Figure 4 shows the mechanisms relating metabolic acidosis with bone disease3. These observations suggest that uncorrected metabolic acidosis has adverse consequences on bone anatomy and physiology.

Figure 4. The various mechanisms by which metabolic acidosis may contribute to bone disease. (From3).

From here, your questions can be answered:
Q: By consuming acidic foods, could one cause their blood to become acidic and therefore cause an acid+base reaction between their blood and bone?
A: Maybe. It is possible to induce a metabolic acidosis with diet:

Adeva, Souto. Diet-induced metabolic acidosis. Clinical Nutrition. 2011. 30(4),416-21.

The modern Western-type diet is deficient in fruits and vegetables and contains excessive animal products, generating the accumulation of non-metabolizable anions and a lifespan state of overlooked metabolic acidosis, whose magnitude increases progressively with aging due to the physiological decline in kidney function. In response to this state of diet-derived metabolic acidosis, the kidney implements compensating mechanisms aimed to restore the acid-base balance, such as the removal of the non-metabolizable anions, the conservation of citrate, and the enhancement of kidney ammoniagenesis and urinary excretion of ammonium ions. These adaptive processes lower the urine pH and induce an extensive change in urine composition, including hypocitraturia, hypercalciuria, and nitrogen and phosphate wasting.

And there is existing research on short-term effects of altered diet on blood and urine pH and composition, but the clinical relevance of these values is indeterminate:

Buclin, Cosma, Appenzeller, Jacquet, Décosterd, Biollaz, Burckhardt. Diet Acids and Alkalis Influence Calcium Retention in Bone. Osteoporosis International. 2001. 12(6),493-99.

The urine-acidifying properties of food constituents depend on their content of non-oxidizable acids or precursors. Acidifying constituents such as animal proteins may negatively affect calcium metabolism and accelerate bone resorption, thus representing an aggravating factor for osteoporosis...acid-forming diet increased urinary calcium excretion by 74% when compared with the base-forming diet (p50.0001), both at baseline and after the oral calcium load, and C-telopeptide excretion by 19% (p=0.01), suggesting a skeletal origin for the excess calcium output. This observation confirms that renally excreted acids derived from food influence calcium metabolism, and that alkalizing nutrients inhibit bone resorption. Further studies are needed to determine the clinical impact of dietary counseling for avoiding diet acids as a preventive measure against osteoporosis.

But best recent evidence does not support the idea that significant changes in bone composition could be induced by diet alone (see my "Short Answer" above).
Q: ...what salt would be produced?
There are many metabolic acids, but for simplicity, we'll consider H+. Bone bases are stored as alkaline salts (e.g. calcium carbonate, CaCO3, which is really Ca2+ and CO32-). So, if H+ comes into contact with calcium carbonate, you'll make carbonic acid (with H+ displacing Ca2+ to produce H2CO3 – you excrete the Ca2+, resulting in the hypercalcuria described above). Through the bicarbonate buffer system,  that H2CO3 will be converted into carbon dioxide and water, which you excrete from your body via respiration.


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Is it possible to identify the wasp species/family by the nest?
I've seen a weird looking wasp nest recently.
Here's the picture:

I'm saying weird because it's the first time I see a nest that isn't a ball made of grey paper. Although this one is also made of paper, I don't understand where does the colour come from.
Is it possible to say, what species or family does it belong to?
(location is the North-West of Russia, close to Saint-Petersburg)

Ok, my bad. Should've googled better.
It seems that it might be a common wasp aka Vespula vulgaris. It's said that the colour of the nest is caused by material being collected from the rotten tree trunks.
See the identified sample:

It's said that they don't make nests in houses too often that's why I'm not accustomed to the look of the nest.


text:
Insect with Mohawk-style back in Mexico City
About 5mm long. Any idea what it is?


text:
Why do many cells together survive better than one cell alone?
I know that one cell with no ECM is subject to anoikis. That's why in general one cell alone not in its environment is dying.
But are there advantages for a cell to live close to other cells even of the same type (for many types it looks obvious) ? If yes what are they and could you give a reference if it is possible please ?
I don't mean only what evolutionary advantages do cells together have over one cell (which is more simple, and there is a wikipedia about it), but I'm more interested if one wants to culture cells that you find generally in tissues, why is it better to take many of them (because it is better, right ?) ?
To be clearer, my point is that I want to understand the mechanisms of what happens when cells (of the same type) are in community and to understand given those mechanisms the advantages a cell has when it is with other cells rather than alone.
Thanks !

Some cells need contact for survival. Is your question about why such a need even exists? I would guess that many cells have to form a uninterrupted layer for performing their function (for e.g. epithelial cells).

@WYSIWYG Could you give me a reference like a book or something plz ?

It's not really clear what you're asking.  There are certainly a great many single-celled microorganisms that survive perfectly well on their own.

@jamesqf well I'm talking about cells that one can find in tissues in general.

@J.A you haven't still clarified if you are looking for the "how" or the "why". BTW, have a look at this article for some info on "how". You can find more articles on Google Scholar.

Thx ! The question is more "how". Actually I understood that the "why" you were talking about was more an evolutionnary point of view. My point is that I want to understand the mechanisms of what happens and to understand given those mechanism the advantages a cell has when it is with other cells rather than alone.

@J.A okay.. Then I shall convert my comments to an answer soon. You also please [edit] your question to highlight that you are looking for the mechanism.

Cells can communicate with each other using chemical signals.
But do you also know about gap junctions? These are tunnels that connect cells in tissues.
Water, ions etc. can travel to and fro.
Or maybe a tight junction can connect cells together to form an an organ. No fluids pass through, which is good: The bladder is an example.


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If one of eyes is blind, can that eye still feel pain?
I was wondering this when I touched my bare eye (my eye was open) and since I'm not blind I was wondering if an eye is blind, can it still feel pain?

Blindness can be due to a damage of the lens, retina, optic nerve or the visual area at the occipital lobe of the brain, for example.
Sensitivity of the eye cornea is enabled by a different nerve - the ophthalmic nerve, which is a branch of the trigeminal nerve (Yale Journal of Biology and Medicine). As long as this nerve, somatosensory cortex at the parietal lobe of the brain and other neural structures involved in pain sensation are intact, you should be able to feel pain when touching the cornea of the blind eye.


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Can you find the amount of heterozygotes in a pop. from the phenotypes shown in the pop
I know the hardy Weinberg equation but that is for the amount of alleles not the amount of phenotypes. So if there are 600 black(dominant) organisms in the population and 400 green(recessive) organisms. Can you figure out how many of the blacks are actually heterozygous?

No one want to do your homework for you.  You will get far better answer if you show what you think the answer is and why.

In short, you would need to know the genetic architecture underlying your trait. How many loci? How does each allele contribute? In your question, you seem to assume that there is a single bi-allelic locus with a simple dominance relationship (where black is dominant). Then yes, you can. What have you tried? You will find the answer in the post Solving Hardy Weinberg problems

Number, not amount. If you need help with your English you may find the following example useful: “amount of sugar, but number of lumps. This is not pedantry — in science precision of expression matters.


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Do birds grieve and feel emotion?
Crows are surprisingly clever with tool making/use and even understanding displacement water over sand! Clearly there's some relatively high level cognitive processes going on up in those avian brains.
When I stumbled across a video of what appears to be a bird grieving over its mate (shown in clip below), I wondered how far animal emotion and psychology goes.

Is that bird in the video grieving? (and shaking because of stress?)
What species of bird is this?

note birds do grieve, this is just not an example of it. https://psycnet.apa.org/record/1993-98443-000

@John: How is it possible to know?  It's certainly possible for humans to grieve without displaying outward signs, or to counterfeit what we see as signs of grief while not feeling the actual emotions.

@jamesqf first grief has physiological and neurological signs, it is a defined behavior, second out of the two options that the birds are grieving or they acting like they are grieving on the off chance a researching is looking the former is vastly more likely than the latter.

Your "grieving bird" is a video of a peregrine falcon (Falco peregrinus) and its (nearly?) dead chick on a hot summer day in Phoenix, Arizona (USA) in 2016.

 Photo credit: Arizona Game And Fish Department
The video is from a nest camera webcam set up in the Maricopa County building in Phoenix, Arizona by the Arizona Game and Fish Department. (See this video for more information). The camera was active in 2016, but according to here the falcons did not return to the nest in 2017. Your video shows one of the adult birds with the only chick that hatched (out of 4 eggs) in 2016. That chick died from a combination of heat and an 8-story fall in June 2016 [Source]. Your video is an edited and audio-less version of a video capture of the live stream that can be seen on Youtube. The information for this video indicates that the adult bird in view is the father.
The adult falcon in the video is not whimpering, crying, or grieving. Instead, the bird is trying to cool down on a hot day. He is displaying a familiar temperature regulatory behavior: panting.
From Bartholomew et al. (1968):

Most birds pant when subjected to heat stress...

In fact, in the more complete video I link to above (with audio), you can clearly hear the bird making panting sounds while breathing heavily.
The falcon also spreads out its wings to better help cool himself down toward the end of the video as it cares to its injured chick.
You can see another video of a panting falcon in New Hampshire (USA) here, and you can find more information about panting, gular fluttering, and other thermoregulatory behaviors in birds here, here, and here.

(+1) Far more believable explanation than grieving.

Most animals have some shared reactions to anti-stress drugs and painkillers, for example it has been proven that lobsters react to the same painkillers as humans in response to stimuli.
Birds are much closer and have a lot of shared characteristics with humans, fear, heart rate changes, adrenaline, stress. There are many studies about general stress, for example: https://www.pnas.org/content/early/2017/06/06/1706164114
That doesn't mean that birds form strong bonds with their children. Penguins have been observed to nurse and prod frozen babies to try to revive them. Complex social emotions have not been strongly proven with most animals, mostly primates, dogs, elephants. Parrot owners will tell you that paired parrots often mourn, lose appetite and die, after their partner dies. They also try to defend their babies with agression. So we can't rule out that birds have parasympathetic nervous reactions similar to our own. humans bite their nails, birds pluck their feathers! https://www.thesprucepets.com/do-birds-get-depressed-390405
You should check this TED talk, about animal psychology:
https://www.youtube.com/watch?v=-wkdH_wluhw

There seems to be a long folk tradition that birds do grieve:

“All the birds of the air fell
a-sighing and a-sobbing
when they heard the bell toll
for poor Cock Robin”

See the Wikipedia article on Cock Robin.


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How to determine if two mutations in a gene are on the same or different alleles?
I would like to know, except a familial study, is there another way to determine if a mutation/variation is cis or trans (i.e. on the same or different alleles)? For example by sequencing technique or other molecular biology procedure.
CIS               TRANS

+  +              +  +
|  |              |  |
A  |              A  |
|  |              |  |
B  |              |  B
|  |              |  |
+  +              +  +

Thanks

Yes, it can be determined by sequencing but the sequencing read has to be long enough to span both the mutations. PacBio sequencing allows long reads but it also has higher error rate than the short read sequencing platforms like Illumina. If you know the gene locus then you can amplify the region using PCR and use Sanger sequencing too (for this the amplicon has to be cloned in a plasmid, transformed into bacteria and then single colonies must be sequenced; see Why does one combine PCR and cloning as ways for amplification of sequences?).
Another possibility is to look at the RNAs from this gene. If the two alleles have different expression then comparing the number of reads for each mutation might tell if they occur together. However, as I said it already depends on the two conditions: expression and dissimilar expression.

Thanks for your reply. So, the family study seems to be the easiest and the cheaper method if both mutation are far away.

@dridk There are some problems with family study: the two mutations may not have linkage and can segregate during crossover. Also, if you want to know about the current generation you might have to wait for them to have offspring. You need data for all of the family members. Moreover, if you don't have a very distinct trait associated with the different mutations then you would again have to rely on sequencing; so back to square one.


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Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?
Some people who get directly struck by lightning and some more than once (starts at 00:25) survive while others die instantly or later on due to complications/injuries.
Looking at a wiki page for Lightning injuries

Lightning injuries are injuries caused by lightning strikes.
They result from three factors:

electrical damage.
intense heat.
the mechanical energy which these generate.

While sudden death is common because of the huge voltage of a lightning strike, survivors often fare better than victims of other electrical injuries caused by a more prolonged application of lesser voltage.

Lightning can strike or injure humans in four different ways but I'm going to focus on direct strikes.

Reported mortality rates range from 10–30 percent, depending on the source of data. Most people who are struck by lightning live to tell the story, but many suffer from long term injury or disability.
  Airforce medicine site

Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?

There is a very wide range of energy in lightening strikes.

To expand on @blacksmith37 comment: being "struck" by lightening doesn't necessarily mean  a direct hit on your person. Even if lightening strikes several yards away you may suffer from electrical shock and be stunned from concussion. In general the further you are from ground zero the less likely you are to be injured, but even then the nature of the local terrain may strongly affect the resulting ground currents, which can be lethal.

Yeah "struck by lighting" covers a fairly wide range of occurrences, including different type of lighting and different types of strikes including direct and indirect. This is like asking why all burn victims do not die as if a first degree burn on the hand and a third degree burn across the entire body was the same thing.

Specified question to direct strikes only.

That youtube video looks like a hoax, though. The camera should have picked way more light based on the distance from the lens to the strikes. Different google search results suggest it may be fake too.

Is there a physiological reason why direct lightning strikes are not lethal for everyone or does it all come down to dumb luck?

To be lethal a lighting strike has to do enough damage to a critical organ that the injury is not survivable.  Since electricity can take highly variable paths through a body, the amount of damage inflicted is also highly variable.
For example, current entering on the head and exiting on the foot stands a good chance of passing through both the brain and heart.  This is likely to be a very severe injury.  Conversely, current entering on the left hand and exiting on the left foot does not cross the body and may leave superficial burns but limited internal injuries.

Lightning strikes the ground which then conducts to you.
By keeping minimal contact with the ground, you give the electricity less of a chance to conduct to you. And if your heels touch, this gives the electricity a shorter path to travel.
It is also important to avoid conductors, such as metal items.


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Sleeping Pill Overdose
How does an overdose of sleeping pills kill?
What are the body's reactions to an overdose?
In an article published in ScienceDaily, I read that "Sleeping pills owe half their benefit to the placebo effect".
So what constituents of a sleeping pill, when taken in excess, lead to a negative reaction?

Note that "Sleeping pills owe half their benefit to the placebo effect" is a statement about the efficacy of placebo for helping sleep; it says little about the actual effects of the drugs and does not mean that sleeping pills are just placebo and does not mean they do not have physiological effects.

Some hypnotics — the active component of sleeping medications — act as central nervous system (CNS) depressants, which in turn depress breathing or respiration, especially when mixed with other drugs, such as alcohol.
If your breathing slows sufficiently and is arrested, as can be caused by an overdose of CNS depressants, your vital organs will be starved for oxygen, which in turn can lead to brain damage and — ultimately — death.

(+1) Piggybacking to say you'd have a vicious cycle of respiratory depression reducing blood oxygen saturation, causing ischaemia and poor perfusion in the respiratory centre (RC), killing the neurons there and in turn causing more respiratory depression. At some point, when all your RC neurons are dead, you stop breathing completely. This would be after the death of other areas of the brain due to the extensive blood supply of the RC. Also I'd note that most hypnotics depress the CNS by facilitation of GABAergic transmission.


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What species of butterfly/moth is this please?

What species is this please?
It's really tiny. That's an oregano leaf.
Location: United Kingdom

Mint moth. We can only see the forewings on this photo. Single gold spot is the giveaway.

Hi Phil. Thanks for providing an answer. Please provide more detail and links/citations to reputable sources that support your claim (and preferably a picture from a reputable source as well). Unsupported and one-line answers will be downvoted or deleted. Please edit accordingly.


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How exactly does symbolic language for apes work?
I'm talking about the panels with lots of colored symbols on them you sometimes see in documentaries and the like. Apes point at the symbols in a specific order and in this way can communicate with humans.
I already googled around a lot, but wasn't able to find any detailed explanation on how exactly the language works (meaning of all the symbols, grammatical structure of the language and so on). It might just be because I don't know what words to use for my search, so can anyone with more expertise in the field point me in the right direction?

The best article I found was this one. In it it says among other things that:

Kanzi, an unusually intelligent Bonobo chimp trained at Georgia State
University, was remarkable in that he learned to use around 200
symbols on a portable electronic symbol board, a computer with buttons
in the shape of absolute arbitrary symbols rather than manual signs.
More interestingly, Kanzi learned how to use this board while watching
his foster mother, Matata, being taught by traditional reinforcement
methods. So Kanzi did learn how to use arbitrary symbols without being
taught, although he did observe direct reinforcement of each symbol
during the process and the symbols were taught one at the time.
The
evidence for the mastery of syntax is not so convincing. While
chimpanzees can learn to order their symbols to get what they want, it
is not clear that they have mastered syntax. The reason is that when
they initiate communication, even adult chimps often abandon the order
they have learned and phrases such as, "Fight mad Austin," a famous
utterance of Kanzi's friend Panbinisha. Here the order doesn't seem to
matter. Apparently Panbinisha was trying to express, "there was a
fight at Austin's and someone (Austin?) was mad". It is interesting
that even human children simply don't make such errors once language
acquisition begins, and certainly adult speakers would never utter
such strings. Notice it lacks any morphemes (-ing, at, I, she, -ed),
the hallmarks of grammar.

The trainer of Kanzi has published some materials but I do not know if they are available free online. You could probably send her an email and ask. The article goes on to state:

The maximum number of lexeme symbols (simple nouns, verbs, and
adjectives) is interesting, too. The brightest chimpanzees master
fewer than 200 of these symbols by adulthood. Human children know
about 50 by the time they are 18 months old, when they begin learning
nouns, verbs, and adjectives at the rate of about 5 per day. So the
maximum achievement in symbol acquisition among other primates is more
than matched by human children before the onset of language
acquisition. In fact, the type of phrases spoken by chimpanzees and
gorillas also resemble those spoken by children before they acquire
their first language: "give orange" or "give Bobby orange" (without
the pronoun me) are common expressions of children before the onset of
language learning around the age of two.
The results suggest that
while chimpanzees and gorillas are far more intelligent than anyone
had imagined during the first half of this century, they are not
capable of human language. Rather, they have a primitive version of
the semantic ability children use before that explosion of
language-learning around the age of two.

At least according to that article there is not much of a grammatical structure at all. The apes does not so much care about the order of the words either, even if the can learn a certain order, especially if they get something to eat if they do it right.


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Edible and non-edible leaves
For humans, what's the difference between an edible leaf like lettuce, and a non-edible (in the sense of null nutritional value) leaf like grass?

What would the answer to this question help you achieve?

What context are you looking for, digestibility, why one is more palitible, what selective pressures make humans not think grass tastes good. Because as it stands the answer is "one tastes good and the other does not" Please flesh out your question, also show some attempt to answer the question yourself as "homework" questions are considered off topic without it.

For grasses leaves tend to be inedible due do with the high quantity of silica deposited in the leaves to form structures known as phytoliths Wikipedia.
While this has been shown to inhibit digestion by insects (Hunt et. al., 2008, Massey et.al., 2006), I'm not aware of any studies on how this affects digestibility for humans.  There are however anecdotes about people starving to death with grass stains around their mouths during the Irish Potato famine.

I'm not convinced the ability of humans to subsist on grass is due to inhibition of digestion; I think it's more likely that we wouldn't be able to digest the carbohydrates in grass anyway. It doesn't seem likely to me that high quantities of silica would be the major limitation of us digesting something. Grazing animals manage just fine on grass, albeit with adapted digestive systems.

@Jam
I'm not aware of a significant difference in the types of carbohydrate present in grass  leaves vs. those of "edible" leaves like lettuce.
However, there is some research showing that silica inhibits both palatability and digestibility for grazing mammals (Shewmaker et. al., 1989, Hartley and DeGabriel, 2016).

Nutrient content of lettuce and grass can be similar.
According to USDA.gov, 100 g of green leaf lettuce contains:

Protein = 1,4 g
Digestible carbohydrates = 1.5 g
Calcium = 36 mg
Potassium = 194 mg
Magnesium = 13 mg
Fiber (cellulose or similar) = 1.3 g

According to Feedipedia (see Nutritional Tables), 100 g of Bahia grass contains:

Protein = 3.5 g
Digestible carbohydrates = 0.6 mg
Calcium = 160 mg
Potassium = 400 mg
Magnesium = 27 mg
Fiber (cellulose) = 7.8 g

The "leaves" (shoots) of most grasses are considered inedible, because they:

are unpalatable
are hard to chew because of high cellulose content
can probably make you sick; at least it can make dogs vomit (PNAS)
contain silica that can wear your teeth; some types of grass are also toxic (eattheweeds.com)

Would it make sense to eat grass in a survival situation? No, because 100 g of grass contains only about 20 Kilocalories, mainly from protein and a little bit from cellulose fermentation by intestinal flora in the colon (gut.bmj.com). It's also quite possible you would vomit or get diarrhea after eating grass.

I don't know if all those things are true (i.e., I'd want to see a reference for having the same amount of micronutrients, differences in chewing difficulty) but in any case that comment I think is much closer to answering the original question. I'll clean up this comment thread.

https://ndb.nal.usda.gov/ndb/foods/show/11253?fgcd=&manu=&format=&count=&max=25&offset=&sort=default&order=asc&qlookup=Lettuce%2C+green+leaf%2C+raw&ds=&qt=&qp=&qa=&qn=&q=&ing=

Good answer but the Daily Mail isn't a particularly academic source.

@Jam, OK, it is known that dogs and cats eat grass to make them vomit when they are sick; there are literally no studies that would even mention eating grass by humans.


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What are names of the colon delimited fields in this FASTA header?
The human chromosome DNA data in Ensembl release 96, here is in FASTA format.
Reading the Wikipedia article on the FASTA format, I understand the first line, prefixed with >, is variously referred to as a "comment" or "sequence headers". However, looking at FASTA files from different sources, it appears this first line is quite variable in actual content.
What are the colon separated fields in this FASTA header (as found above on the Ensemble FTP site)?  Most fields are guessable, but an explanation of each field would be much appreciated.  I believe the 46709983 is the number of base-pairs in the chromosome.
>21 dna:chromosome chromosome:GRCh38:21:1:46709983:1 REF
Finally, how should I have figured out the meaning of the header notation for myself?  Is there a list of common or known header formats?

According to ensembl's website (albeit somewhat buried in a page about downloading data via FTP) it says:
"The header line in an FASTA dump files containing DNA sequence consists of the following attributes : coord_system:version:name:start:end:strand This coordinate-system string is used in the Ensembl API to retrieve slices with the SliceAdaptor."
A brief rundown of these attributes as I understand them:

coord_system- Is simply the coordinate system used to locate a particular feature within an assembly: "chromosome" and "BAC clone" are common examples as described here.
version- This is the current version of the assembly reference. And refers to an Ensembl archive as detailed here. (Yours appears to be from the human GRch38 assembly).
name- This seems pretty self explanatory. In this case we are looking at chromosome 21.
start- Again, self explanatory. Any complete chromosome or contiguous sequence is going to start at "1".
end- End of the fasta sequence. [start] - [end] + 1 = total length
strand- This refers to orientation (i.e. forward or reverse strand) 1 is forward (-1 is reverse)

Here is a link to a pdf containing this information and more about using Ensembl (see page 23)...
Unfortunately, to answer your final question, there is no easy way to come across this information and there are as many ways of labeling fasta files as there are sequence databases. Sequence repositories have come a long way in the last 10 years but there is still a lot of work to do toward standardizing data formats and making databases more user friendly.

Thanks David. I had looked at that page last week, in fact (it was helpful to know Ensembl supports rsync), but not read it closely enough, evidently. Cheers!

@RichardMichael fasta header can be anything. It is flexible because different fasta files would have different kinds of sequences. Therefore one standard will not suit them all. Moreover, fasta header is not really meant for annotation. If there is a GTF associated with the fasta then you will have the genomic co-ordinates and some other information (for e.g. the gene name) in the former.


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Why do some people have symptoms of salmonella and others not?
So I was reading from the Mayo Clinic website and they say that typically people with Salmonella have no symptoms, but why?  Why do some people have symptoms and others not?  Salmonella does after all mutate.
Here is an excerpt from the Mayo Clinic Website

"Typically, people with salmonella infection have no symptoms. Others
  develop diarrhea, fever and abdominal cramps within eight to 72 hours. Most healthy people recover within a few days without specific treatment."

https://www.mayoclinic.org/diseases-conditions/salmonella/symptoms-causes/syc-20355329

I removed the "toxins" tag because salmonella doesn't actually secrete toxins like Clostridium. Anyway, why is this fact difficult for you to understand; people have varying levels of immunity to different pathogens. Can you elaborate more on what you specifically want to know?

Symptoms can also depend on the number and virulence of the Salmonella bacteria you ingest.


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Why is double stranded DNA considered to be one molecule?
Wikipedia, for example, refers to DNA as "a" molecule, not two separate molecules forming a double-helix structure. Isn't this technically incorrect? There are two separate polynucleotide strands (each that can be considered one molecule on its own as the monomers are joined together by covalent bonds), and the strands joined together by hydrogen bonds and not covalent/ionic bonds along their length. Doesn't that exempt them from being considered one molecule, as the bonds joining them are intermolecular and not covalent or ionic?

If we considered a double-helix to be two separate molecules, then how do describe two separate double-helices? I think using the singular "molecule" with a double helix is appropriate because it makes it easy to use the plural "molecules" when referring to a group of DNA double-helices. Also, there are other supramolecular complexes such as Catenanes and Rotaxanes which are generally referred to as singular molecules despite having no covalent bonds between the parts.

DNA is a molecule. dsDNA is a supramolecular structure. Wikipedia is not the authority on biochemical nomenclature. You can edit Wikipedia to correct this.

I'm voting to close this question as off-topic because it is about the correctness of a wikipedia article. The question may also become invalid if wikipedia is corrected.

Also, it is a possible duplicate of https://biology.stackexchange.com/q/66343/3340

Wikipedia was just an example. The answers to the question linked seem to say that DNA is one molecule. The text referenced in Charles' answer (Molecular Biology of the Cell) says one, single DNA molecule is 2 polynucleotide chains, just like Wikipedia. I find the answer abut DNA being a polyatomic ion/2 polyatomic ions to be the most accurate, since a molecule is by definition uncharged (or only partially charged).

@BillWilson — I look forward to your next publication in which you refer repeatedly to DNA as a complex of two polyatomic ions. The ion thing is irrelevant anyway (it is always balanced by cations) and you have essentially the same problem with haemoglobin. How are you going to refer to that? I think you need to emerge from your chemist’s cocoon and think about the state of science when, and the purpose for which, the term “molecule” was devised. Compare that with the state and purpose today, and the practicality of using words to communicate ideas.

@Bill Wilson The word "molecule" is usually meant to describe a "thing" on the atomic scale. Even the IUPAC definition essentially says a molecule is an "entity" bigger than 1 atom (note the lack of bond types). https://goldbook.iupac.org/html/M/M04002.html.     The reason why dsDNA is called a molecule is likely because the two strands behave as one entity in physiological contexts.

For all intents an purposes dsDNA "entities" will behave as a single molecule when handled in the lab unless you heat them above melting temperature or add chemicals and reactants that modify the strands.


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Species Identification

I found this in my hair this morning! Yucko! Please help me identify it. I have tried and tried to no avail.Thanks in advance.

What size is this? And where in the world are you located?

This appears to be an insect head; without the rest of the animal any identification is going to be suspect.


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Water potiental

I think solution x should be present at Z as this solution has moved out of cell causing cell to be plasmolysed but the answer is Y. How?

It is not solution X what is going out of the cell, but the solvent (water) of solution X.
Also, you need to keep in mind that the cell wall permeability is by far less selective than the cell membrane. This is why solution Y can diffuse freely to Z.


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Number of dopaminergic neurons in VTA
Do you know an authoritative source for the approximate number of dopaminergc cells in the ventral tegmental area (VTA)?
Ideally I would like to know this for mice, rats, as well as humans, but one species alone would be a nice start. I have looked for this via google scholar and pubmed, but found nothing.

Integrating the information from @WYSIWYG's excellent answer, it appears the dopaminergic neuron count lies at:

4k for mice - Triarhou, 1988
10k for rats - German and Manaye, 1993
250k-440k for humans - Rice et al, 2016

Approximately, 250000-440000 neurons in Humans (Rice et al., 2016).

The substantia nigra/ventral tegmental area (SN/VTA) complex is a
  heterogeneous collection of dopaminergic cell groups that extends from
  diencephalic to mesencephalic territories in many vertebrates,
  including rodents, non-human primates, and humans (Puelles and Verney
  1998; see as reviews Smits et al. 2006; Smidt and Burbach 2007; Smits
  et al. 2013). The SN/VTA contains the largest number of dopaminergic
  neurons in the brain (see as reviews van Domburg and ten Donkelaar
  1991; Haber and Fudge 1997; Nieuwenhuys et al. 2008), with average
  estimates ranging in most studies from approximately 250,000 –
  440,000 dopaminergic neurons within the complex (Bogerts et al.
  1983; Hirsch et al. 1988; van Domburg and ten Donkelaar 1991; Damier
  et al. 1999a; Kubis et al. 2000).

Thank you. Any ideas about the other species?

@TheChymera no idea. I'm also relying on Google scholar and pubmed. I have no expertise in this field.


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Has anyone confirmed Darwin's theory that nectar began as something "injurious" to sap?
In "Origin of Species", Darwin says (I have added bold for emphasis):

Certain plants excrete sweet juice, apparently for the sake of
  eliminating something injurious from the sap: this is effected, for
  instance, by glands at the base of the stipules in some Leguminosae,
  and at the backs of the leaves of the common laurel. This juice,
  though small in quantity, is greedily sought by insects; but their
  visits do not in any way benefit the plant. Now, let us suppose that
  the juice or nectar was excreted from the inside of the flowers of a
  certain number of plants of any species. Insects in seeking the nectar
  would get dusted with pollen, and would often transport it from one
  flower to another. The flowers of two distinct individuals of the same
  species would thus get crossed; and the act of crossing, as can be
  fully proved, gives rise to vigorous seedlings, which consequently
  would have the best chance of flourishing and surviving.

My first question is, has anyone done any experiments or chemical analysis or any other kind of science to show that nectar does in fact contain something "injurious" to the sap (or to the plant in general)?
More importantly, has anyone tried to "prove" Darwin's theory of the evolution of nectar in flowers?
I understand that Darwin seems to provide some hints by mentioning the

Leguminosae, and at the backs of the leaves of the common laurel.

as examples of a plant removing toxic substances from somewhere other than a flower, but I'm wondering if someone has "proved" that nectar in flowers started as a toxic substance the plant needed to remove.
Additionally, I'd be interested in how plants that haven't developed nectar/flowers deal with this waste (other than the common laurel and Leguminosae).  For example, does the plant just store the waste in a vacuole until it dies (please pardon my bad biology if "vacuole" isn't the correct organelle -- I'm not a biologist)?


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Why does K+ going out of the cell cause hyperpolarization?
I'm really  confused by how the terms Hyperpolarization and Depolarization are used in Cell biology and hope somebody can enlighten me hopefully.
Here's what they mean for me so far:
Depolarization means the inner and outer side of the cell membrane become less polarized (so the Nernst potential tends to 0 due to log(1) being 0)
Hyperpolarization that the inner and outer side become more polarized (so the Nernst potential increases).
Assuming I'm not completely wrong until here.
Let me give some examples, so maybe you can see better where the problem lies:

We have a model cell so (K+ internal is 140 mmol/l, K+ external is 4.5 mmol/l) and the external side is increased to 8 mmol/l , then a DEPOLARIZATION occurs because

roughly : $-60 \cdot \log(140/4.5) = -90 mV < -60 \cdot \log(140/8) = -74 mV$ ; or in other words, "energy" was used so a depolarization occurred (so far this seems correct with the solutions I can find to this example)
\
\

Now comes the second example (famous depolarization of a cell with the graph and the peak and repolarization):

Na+ enters the cell : the concentrations im gonna use for this example are inside:$12 mmol/l$ and outside $140 mmol/l$

so before the Na enters we have: $-60 \log(12/140)= 60 mV$
if Na+ enters the Cell, a depolarization should occur (because the difference inside and outside is decreased)
this seems fine with the graph...

the part of the graph which goes over 0 (also called "overshoot"), is it not technically a hyperpolarisation+depolarization?
repolarization: this occurs by K+ ions leaving the cell, but that doesn't make sense according to the Nernst equation?

The concentration inside before the cells leaving is 140, outside 4.5 ; if K+ leave the cell, its simply going to depolarize more... So why does repolarization occur and not depolarization?

It's commonly stated that Hyperpolarization is caused by K+ LEAVING the cell (for example with ion channels) , how does this make sense if the inner concentration is higher than the outer? If anything, this again should lead to depolarization
Same thing with K+ entering the cell, isn't that supposed to cause a hyperpolarization as well?

I appreciate any kind of insight into this matter, since it seems that I'm completely wrong.

Why do you think that K+ leaving the cell is going to depolarise more? When Na+ enters the cell, it affects the total ionic concentration inside the cell, so that Na+ entering the cell (depolarisation) is “balanced” by K+ leaving the cell (repolarization). You also have to consider that a lot of channels are voltage-gated, so they regulate ionic transport based on a change in total membrane potential, regardless of which ion concentrations caused the change in potential.

considering the Na+ entering is probably smart BUT for example; if you have a cell why is it said that K+ leaving the cell will cause hyperpolarization? if it is not true due to the Nernst equation ? Same with K+ entering the cell ; regardless of whether Na enters or not ; if K+ leaves the cell potential from nernst will go towards 0 ; yet it is still claimed that this will cause a hyperpolarization? Is my understanding of depolarization and hyperpolarization incorrect?

since cell membranes are normally polarised at a resting potential of -70 mV, hyperpolarisation refers to any event that polarises the membrane even more, making the cell interior more negative beyond -70 mV (so the opposite of depolarisation). Hyperpolarisation is not specific to K+, and K+ leaving the cell doesn’t necessarily cause hyperpolarisation: it only does so when potassium channels stay open for a longer duration, allowing more K+ to leave the cell than needed to repolarise the cell back to -70mV.

The extra efflux of K+ and hyperpolarisation are important concepts in neurons, because nerve cells can only be excited (depolarised) from their resting potential. Going from a hyperpolarised state to the resting potential of -70mV allows a gap in time between excitation events. Because you wouldn’t want neurons firing constantly! :)

How does that relate to the simplified Nernst equation? I don't really see how your comment answers my question: $\frac{-60}{k} \log (C_{in}/C_{out})$. If you go from 140 inner  and increase the concentration outside, then according to the equation it's going to go towards 0 ; this by definition is a depolarization ??????

K+ and Na+ movements across the membrane are coupled in cells, so I think you need to use the Goldman equation instead of the Nernst in order to account for both ions.

So when somebody says K+ is leaving the cell, what they really mean is Na+ is entering at the same time which in total causes a hyperpolarization?

Yes, that is exactly my reasoning.

My answer: it's not the concentration change that causes repolarization, it's the permeability change.
The relevant equation here is the Goldman-Hodgkin-Katz equation, which entails that transmembrane voltage V_m is proportional to the ratio of [K]_o/[K]_i times permeability P_K:

[K]_i is always higher than [K]_o, so the ratio of [K]_o/[K]_i is always providing a negative contribution to V_m. During repolarization, the contribution from this ratio becomes less negative as its electrochemical gradient evens out, and if this was all that was happening then V_m would increase. However, there is a second relevant term that changes upon repolarization: potassium's permeability. P_K increases dramatically during repolarization, providing a negative contribution to V_m.
Note 1: Because potassium is positive and the cytoplasm is negative, the electrochemical gradient favors [K]_i > [K]_o. This explains why the transmembrane voltage decreases to -90 mV instead of 0 mV.
Note 2: The only reason why Vm is positive during an action potential in the first place is because there exists a high resting [Na]_o, and so a step change increase in sodium's permeability P_Na is what's driving the AP Phase 0 increase. As soon as P_Na drops, we would expect V_m to drop too regardless of what's happening with potassium.
Note 3: While I think your definitions make more sense (i.e. they're more literal), this quote (from Raz 2013: "depolarization is a positive change from the resting membrane potential") implies to me that "depolarization" has shifted from its historical definition to now just mean "an increase in transmembrane voltage".

Welcome to the site!  References would be appreciated.  Thanks!

With respect to "note 3", there's really nothing biologically meaningful or special about the potential "0 mV", hence the use for "depolarization" meaning "any positive change from rest", sometimes including overshoot.

Here is how I think of the issue. First, keep in mind over the course of the action potential, ion concentrations on both the outside and inside of the neuron remain relatively unchanged.  You can think of the Nernst potential as a charged battery, and they keep their concentrations relatively constant. Currents will flow, and the voltage will change, but this effects very few ions at a time, and does not effect the bulk concentration (See section 2.6 here). This is because any small change in concentration near the membrane (where voltage is measured) will quickly equalize with the surrounding bulk solution via diffusion.
Second keep in mind that the Nernst potential is an electro-chemical potential. Thus for potassium in particular, the chemical potential will overpower the electric potential driving potassium out of the cell, making the driving voltage of potassium negative.
So, as you state, the Nernst potential of sodium is $60$ $mV$ and for potassium is $-90$ $mV$. In your example there is a rest potential of $-70$ $mV$ this is given by the GHK potential mentioned in the comments. That means at rest, the balance between the sodium and potassium potentials is $-70$ $mV$. Here is the equation for reference. Note that this equation reduces to the Nernst potential when we consider only one ion.
$$ V = \frac{RT}{F} \ln(\frac{g_{Na}[Na_{out}]+g_{K}[K_{out}]}{g_{Na}[Na_{in}]+g_{K}[K_{in}]})$$
When the action potential starts, the depolarization is driven by the opening of sodium channels, that is $g_{Na}$ gets larger. Thus, when these channels open sodium rushes out and the cell voltage attempts to become more like the sodium Nernst potential, not zero. You can see that in the equation for the GHK voltage equation as the sodium conductance dominates the equation.
Near the peak of the action potential, the sodium channels close, and the potassium channels open. That is $g_{Na}$ gets small, and $g_{K}$ gets large. This means that now the potassium conductance dominates the equation, and the neuron's voltage becomes more like the $-90$ $mV$ Nernst potential. Then the repolarization occurs when the potassium channels close, and $g_{Na}$ and $g_K$ are back to there intial closed values, bring the rest potential back to $-70$ $mV$.
**note I am oversimplifying how the gates change in time, but I think this will help clear up your confusions.

Adding K+ on the outside of membrane is not the same as transfering K+ from inside to outside.
When K+ is added to outside(hyperkalemia) the RMP becomes less negative(depolarisation)
When K+ is transfered from in to out RMP becomes more negative(re/hyperpolarisation)
We should not forget that most of the intracellular anions are nonpermeable protiens, so when K+ is transfered to outside they pull harder, and when K+ added outside, the pull decreases

Can you expand your explanation a bit, as well as expanding the acronyms?


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Can Cas13 be used with multiple crRNAs in the same reaction?
CRISPR-Cas13 equipped with crRNA (complementary to transcripts of interest) can be designed to target ssRNA transcripts in cells.
Upon successful crRNA and ssRNA binding, a fluorescent domain on Cas13 generates a signal, indicating that target has been found.
As far as I know, this method has been used to find one ssRNA target at a time. If we use different wavelength fluorophores for distinct Cas13-crRNA targets, is it theoretically possible to mix them all in the same reaction and distinguish the presence of different targets based on the different fluorescence wavelengths generated during target binding?
In this paper one fluorescently labeled crRNA is used to detect cleavage of one RNA target through complimentary binding. So is it theoretically possible to use several crRNA, each labeled with a different fluorophore, to cleave and detect several target RNAs?

Your link to the paper is broken, is this what you mean? https://science.sciencemag.org/content/356/6336/438.abstract. Also note that you talk both about flouresently labeled CRISPR proteinn (easy to do, but always 'on') and labelled crRNA (hard to do, maybe only signal on binding possible).

As far as I understand it's not the crRNA that is fluorescently labeled, but a cleavage reporter that is mixed into the reaction. The cleavage reporter is not even the direct RNA target, but apparently gets "inspecifically" cleaved as a result of "collateral cleavage". So to me it seems this method cannot be used for multiple target detection.
Paper also at PMC: https://www.ncbi.nlm.nih.gov/sites/ppmc/articles/PMC5526198

Answer is no. Because each CRIPSR-Cas(xx) system works as a ribonucleoproteic complex, so they needs to be loaded with a crRNA in order to be working. Functionality is guaranteed while each of the Cas endonuclease domain is associated with a crRNA. You maybe could use multiple Cas13 with multiple crRNA.
In molecular diagnosis is common to use orthogonal CRISPR enzymes with different crRNA, as can be seen in this original research.

I think your answer is self-contradictory... you said the answer is no but then "maybe could use multiple Cas13 with multiple crRNA", so technically, it's a yes?! My main question was whether it was possible to use multiple crRNA that are labeled with different wavelength fluorophores, so that the signal from target binding could be distinguished based on the color signal. If you look at the paper that I just added in my question, they use one fluorophore to detect cleavage of RNA molecules complimentary to crRNA. What if we use multiple crRNA, each labeled with different fluorophores?

It should be possible, I don't see why not. Just as you can use multiple gRNAs, as long as there is an abundance of Cas13 protein you can target multiple sequences at the same time. So if you, let's say, get a green fluorescent probe for RNA 1 and a red fluorescent probe for RNA 2, you'd be able to distinguish their localization.