text:
How are cells different depending on the ethnic origin?
I recently came across an article about the fact that cell-lines provided by merchant entities to give cells to researchers, were tagged by ethnic origin. The article especially speaks about ethnic origin of African and European. The article points out that the lack of diversity in available cells has consequences on the effect of the therapies made by researchers, since they can work only on limited European (which are the majority of the provided cells). I understand that this concerns stem cells (am I correct?).
I understand of course the problem, but what remains unclear to me is : How are cells different depending on the ethnic origin? (especially protein coats of the cells that affects the vulnerability to diseases) The first answer I have is that they could be distinguished by their DNA (obviously genes coding skin color will be different).
With my researchs I found other articles that gave some information:

This lacks of diversity has an impact on the prostate cancer, so does it mean that prostate cells are different depending on the ethnic origin?
Some viruses have different expression in different ethnic origins

The article is particularly concerned with personalized/precision medicine: tailoring therapy to specific individuals based on their genetic background.
The article is in particular talking not about stem cell lines, but about cell lines derived from patients with cancer. These cell lines are studied to understand what made those cells cancerous, to both understand mechanisms of cancer and develop treatment.

How are cells different depending on the ethnic origin?

The issue raised is not a specific difference, but rather the unknown. If you only study variation among European-derived cell lines, you cannot possibly understand human-wide variation. Further, if you have just one cell line labeled as "African-American" and use studies with this cell line to make decisions about how you're going to treat all Americans with Black/African ancestry, and that one cell line is also mostly of European origin, you shouldn't expect that research to result in good outcomes for African-American/Black patients.
An example of how this might work is that a bunch of study into cancer cell lines identifies some specific mutation associated with cancer, and some pharmaceutical treatment that is highly effective in cancers based on that mutation (perhaps an antibody-based treatment). The next step would be to identify patients who carry that specific mutation or where that mutation is present in biopsied tissue, to give them that customized therapy. However, if all the cell lines you study come from people with European ancestry, only people with European ancestry are likely to have any of those specific mutations, and everyone else is left out.
In particular, African populations are more genetically diverse than populations anywhere else, presumably because humans first evolved in Africa and subsequently traveled elsewhere. Therefore, studying mostly people of European ancestry merely because they are the dominant group in a specific high-wealth country like the US is leaving the majority of human genetic diversity out of study.
The article you linked about prostate cancer seems like a good place to further understand this: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7219314/
It describes how therapies developed because they are effective in a single prostate cancer line didn't actually work for most people with prostate cancer, and that subsequent efforts to study therapies in multiple cell lines have not benefitted "Men of African Ancestry" because those cell lines are predominantly derived from "Men of European Ancestry".

Can you clarify how it comes about that "you have just one cell line labeled as 'African-American'...and that one cell line is also mostly of European origin"? Is it typical or atypical for a cell line from a random African-American patient to be "mostly of European origin"? Are you alluding to a specific cell line (e.g., HeLa)? I do see mention that Lacks's family was mixed-race ("Many of the black Lacks family were also descendants from the white Lacks family"). If that is your point, perhaps you can say it more directly.

@nanoman This is from the article in OP's question, which links to this paper: https://aacrjournals.org/cebp/article/28/6/1003/71948/Genetic-Ancestry-Analysis-Reveals "For instance, the 22Rv1 prostate cancer cell line was recently found to carry mixed genetic ancestry using a much smaller panel of markers. However, our more comprehensive analysis determined the 22Rv1 cell line carries 99% EUR ancestry. Most notably, the E006AA-hT prostate cancer cell line, classified as African American, was found to carry 92% EUR ancestry"

@nanoman Here's another descriptive article you might be interested in: https://cen.acs.org/biological-chemistry/cancer/Genetic-tests-reveal-cancer-cell/97/i10 Overall, though, my answer isn't particularly concerned with testing the premise, and cancer biology or ancestry determination are not my fields. I'm just answering OP's question about why someone would find this concerning and what the implications are for personalized medicine.

Could be a difference between self-reported ancestry, and genetic ancestry. Could be deliberate choice when completing the donation forms, or could be a typo or other accident - click the first choice in a drop down for example. By genetic ancestry, I mean clustering within large-scale population genetics studies such as Thousand Genomes

Thank for the answer, but if the article raised the issue, I suppose it is because the article does not "suppose an unknown difference that would impact the treatment's efficenciency" but because this difference is already a known phenomenon (like we already know that cell X has mutation Y for European but not for African)?
And a subsidiary question: if treatment's efficiency could be that much lowered/increased by ethnic difference, why does'nt it impact viruses or bacteria the same way ?

@totalMongot "I suppose it is because ... this difference is already a known phenomenon" I disagree - the issue is if you don't study both you don't know what the differences are, plus that it is known that there are poorer outcomes for prostate cancer for Black patients. I don't understand your statement "why does'nt it impact viruses or bacteria the same way", my answer does not mention viruses or bacteria.

@BryanKrause For first part I might have wrongly expressed but that's what I meant: some differences like outcome of prostate cancer are already known.
The statement is an extension from your answer: if diseases act differently because of cell differences, do viruses or bacteria act differently as well?

@totalMongot Different people have different responses to viruses and bacteria, yes, both within and between populations.

@BryanKrause Ok but is there a specific ethnic criteria about these differences? As for the previous example of prostate cancer?

@totalMongot What do you mean by "a specific ethnic criteria"? A historical example might include the decimation of populations native to the Americas after exposure to European illnesses, notably smallpox. Sickle cell trait would be another example.

To supplement @Bryan Krause's excellent answer, I would add another with a very specific example of the kind of variation that could affect research.
Different people have very different responses to drugs, and in many cases this variation is genetic. This variation exists across human populations, but can also to some extent be non-uniform or "private" to specific populations, meaning that sampling populations unevenly will give an inaccurate estimate of drug response variation. For example, appropriate warfarin dosing varies dramatically across patients, based in part on genetic variation in known genes.
Thus, if all cell lines tested for response to a new drug candidate are of European descent, then you only understand the pharmacokinetics of that drug for a relatively small sample of overall human pharmacokinetic variation. This could lead to ineffective or lethal (!) drug dose guidance if initial studies in cell lines do not assay a representative range of human genetic variation. (Note: in general, many regulatory safeguards are in place hoping to prevent this kind of event.)
Expert reviews have in some cases explicitly counseled personalized genetic testing to avoid such adverse drug reactions. This indicates that surveys at the population level are in fact inadequate to this problem, as they are too crude. So the issue is not really ethnic population representation, but rather the large scope of human genetic variation, to which apparent/reported ethnicity is only modestly correlated.

Many of the works on "ethnic origin" are based on the chromosome Y. Majority of it (not all) does not have the pair to recombine (very small region still recombines with X), so essentially the same Y chromosome is passed from father to son, different only by infrequent mutations. Using these mutations, it is possible to construct a map of human origins, starting from Y-chromosomal Adam. This would reflect the history about how humans migrated, populating the Earth. The known "versions" of the Y chromosome are called "haplogroups", these are highlighted here by color (image credit):

There are obviously less groups than countries but very approximately this can be matched to the "ethnic origin" in cases like at least Russia, China, India or Australia, and to some ethnic groups that are known to be somewhat tied together, like the European region, for instance. In such cases, the origin of the parent line of ethnicity like Russian vs Ukrainian can be estimated by DNA sequencing of the Y chromosome.
These chromosome signatures cannot be "assimilated" by living for generations in a region where another type of Y is dominant. A hundred generations can pass and the simple scan of the Y chromosome would still show the true origins of the parent line.
There is obviously no reason to think that any version of Y chromosome is better than other. In general there not so many genes there. However anyway the Y chromosome is part of the cell.

The paper referenced in the OP's link is using SNPs from modern populations; so, if you have SNPs that are commonly found in people from Europe, and not commonly found in people elsewhere in the world, you can say you have a high probability of European ancestry. It's the same approach that commercial genome analysis companies offer to individuals. It has nothing to do with the Y chromosome or determining the migration of peoples in history/human origins. This answer also doesn't appear to answer the question asked about how the cells differ/what the concern is in this paper.

Please read the referenced sources, "has nothing to do with Y chromosome"

I'm talking about the OP's question, not your answer.

I think that my answer addresses the question well enough, sorry about this.

@h22 Thanks for the detailed answer. I understand that all (or at least significant part) of the difference between ethnic people is "coded" on the Y chromosome? Am I correct? Also, this means that these specificities are recurrent (not different between me and another guy of same ethnic origin?
PS: I upvoted because even if it focuses on the Y chromosom, it gives hindsights useful for the answer

@totalMongot no, ethnic differences are evenly spread over all chromosomes.

OK so Y chromosom is only one way to follow them. But in what do cells actually differ? Do their cell receptors, proteins differ?

@totalMongot there are all sorts of differences, depending on the genes we're talking about. Some populations with a certain genotype may be more susceptible to damage from a certain environmental toxin, for example, or get a certain kind of cancer more easily than another. The actual physical differences can be found at the protein level, or in the way genes and groups of genes are regulated in different ways due to differences in DNA sequences.

@h22 I honestly don't see how this answer addresses the question at all. OP was not asking about Y-Adam or the origin of ethnic differences at all.

Y haplogroups are good for tracking migration because they're strictly divergent (two Y hapologroups will never merge) and because they accumulate mutations at a predictable rate, giving information about timing.  They're not much good for anything else precisely because of that divergence: every other chromosome can get mixed up with others.  For example, an African-American male might be Y-hapologroup B-M150 (west African) with the entire rest of his DNA being European-typical variants.


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What are the mechanical properties of human skeletal muscle?
TL;DR: I need more information on the mechanical properties of human skeletal muscle; if you have such information, please give it to me.
I'm writing something on how much more effective (or otherwise) spider silk would be as a muscle and/or connective tissue in prosthetics in in comparison to human skeletal muscle and connective tissues. As such, I need information on several of the mechanical properties of human skeletal muscle, such as its:

fatigue limit; this is particularly irritating to attempt to find info on; looking it up instead gets returns on the entirely unrelated concept of muscle fatigue, even with very specific search terms.
ultimate tensile strength; while I have sources for this, they're inconsistent, giving me values between 0.44 MPa and 5.3 MPa - more than an order of magnitude in difference!
tensile and/or compressive (i.e. end-to-end/lengthwise) Young's modulus; I already have information on its transversal (i.e. perpendicular to a strand) Young's modulus, which, from what I can tell, is another word for shear modulus, and therefore is useless for my purposes; after all, good muscles are, AFAIK, supposed to withstand tensile or compressive loads, not the shear ones discussed in that source.
elastic modulus; I already have information on it after 8 days of cell differentiation (45.3 ± 4.0 kPa), or the elastic modulus of the rectus femoris in particular (16.67 to 85.31 kPa, depending on pressure applied), but these sources contrast with one of my sources for skeletal muscle's ultimate tensile strength, which states that this figure is 36 ± 19 MPa.

I was also able to find another source on its Young's modulus, but it doesn't specify the direction the Young's modulus was measured in.
One of the few sources I currently cannot find problems with are this one, on how much a strand of muscle can elongate before it fails - and that's because I can't find any other sources which could contradict it - and this one, on how much force a longitudinal muscle of a certain cross-sectional area can contract with: ~30 newtons per square centimetre, or 300 kPa.
There's also the content of and source of this Biology Stack Exchange answer by WYSIWYG, especially the image displayed:

...although I'm still trying to figure out which parts of it correspond to which points on a stress-strain curve.
The unifying factor here, however, is that I don't have enough sources - so few, in fact, that I have no reliable information on the fatigue limit. Please give me more.

source: Stack Exchange

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

sort: votes


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Can DNA replicate without polymerase?
Would it be possible for short DNA molecules to replicate, for example, if it's heated to the point where the strands separate (as far as I know, that's what happens in PCR?) and freely floating bases could "connect" to their correspondent bases (A/T, C/G)?
I'm assuming that A/T and C/G bases strongly 'attract' each other naturally, perhaps that's where I'm wrong?

Not what you asked, but note that RNA can do this. (See also Wikipedia.)

@IlmariKaronen — RNA Can do what? RNA only replicates in certain viruses, where it requires  a replicase and NTPs. Speculation about replicative capability of primaeval RNA should be described as “might have been able to” rather than “can”.

@David Incorrect, RNA can self-replicate without any other molecule except the nucleic acids it builds itself from. Self replication of RNA was demonstrated over a decade ago. You are confusing Industrial use of RNA replication with what we know the molecule can do. Not only does it replicate it evolves into different linages as well. https://www.labroots.com/trending/cell-and-molecular-biology/22442/self-replicating-rna-molecules-life-arose and https://www.sciencedaily.com/releases/2009/01/090109173205.htm

@John - you make it sound like every RNA species is capable of self-replication. What you actually mean is  "self-replicating machines can be built from only RNA". These are two very different messages.

@markur I make it sound like no such thing.  I'll be crystal clear there are single strands of RNA that fully capable of self-replication, no other machinery needed. No replicase, not even multiple strands of RNA.  just water, ONE strand of RNA and some free floating nucleotides. Literally what the OP is asking for but RNA instead of DNA. no speculation. You are just wrong, RNA "can" self replicate without other machinery. I did provide links read them before claiming I "meant" something.

No, replication cannot happen in the absence of polymerase (on the timescales relevant to humans).
You are correct that in PCR, the first step is to separate DNA strands at 98 C. This heating dissociates the strands semi-permanently. So when you cool down the reaction, the strands do not re-associate very quickly.
When you cool down the reaction to 72 C, A/T and C/G can make temporary connections with their opposite bases. However, the free nucleotides cannot quickly form phosphodiester bonds with the growing chain of DNA in the absence of a polymerase. The nucleotide will most likely dissociate from the DNA strand before the correct bond forms. In other words, it is a kinetic problem.
However, at high temperatures, specialized conditions, and on long timescales, such as those present in earth's pre-biotic period, the answer may be different.

Is it fair to say that the polymerase is mostly helping the DNA to be put together somewhat "in order" (one nucleotide next to the other) so they can form stronger bonds with each other, becoming stable?

Nope. Not happening.
The high temperature (90 °C) needed to separate a DNA strand also makes an association of free floating bases to a template strand much too unstable.
Even if the bases associated with the template strand, they wouldn't spontaneously connect (phosphodiester bond formation) with each other. It needs a catalyst.
Also, it requires not bases, but dNTPs. dNTPs have phosphates (anhydride bonded) that deliver energy to the phosphodiester bond formation connecting each dNTP.

Only one phosphodiester bond is broken during dNTP utilization for DNA synthesis, so talk of three phosphates delivering energy is misleading, to say the least. The point is thermodynamics — provision of energy for phosphodiester bond formation — which bases cannot provide.

The bonds between the three phosphates are of anhydride type, not diester.  I removed "three", since it seems to be confusing.

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


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Can anyone tell me what species this baby bird this is?
Can anyone tell me what species this baby bird this is? He or she is less than two weeks old. Fell out of nest. He is doing well. I live in Sacramento Ca, Thank you.

Looks like possibly a baby starling to me

whatever it is, it probably needs feeding in the same instructions as a baby blackbird or a starling, i.e. every few hours, hard work.


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What determines walking direction in humans?
I've wondered about this for a while, without being able to come up with an answer.
Is there a body part that single-handedly determines the direction we're walking in? Is it a group of body parts that make us "steer" when walking?
I took a look at the behavior of some body parts while walking, and I came to the conclusion that:

it's not the direction the feet are pointed to, as you can turn them in or out while maintaining your path
it's not your head, of course, as you can be looking at any direction while maintaining your path
it's not your hips either, as you can move them freely without changing path (although I wouldn't suggest trying that in front of people)

As much as this sounds like a silly question, I still haven't been able to get to an answer. Any input is appreciated.

the brain which coordinates movements determine directions. You will note you can move in any direction regardless of which way you are facing. Whichever direction your feet are producing the largest net force is the direction you will travel.

Are you asking what part of the body controls voluntary motion?

It's the center of mass of your whole body, projected onto the floor, in comparison to the position of your feet; the center of mass will fall away from your feet, especially from the line that can be drawn between your 2 feet. So walking can be seen as continuous falling.

@KaPy3141: No, or more precisely, not necessarily.  Though what you describe is an efficient way of walking, it's not the only way.  Consider side-stepping (familiar if you're a cross-country skiier), walking backwards, or at a slow pace...

I Agree with @John, the feet that is in the floor generate a force that is going to move your center of mass. The other leg movement is also important because wherever it poses is going to determine the displacement of that step. Of course the rest of the body should move accordingly to achieve balance.

@james: Can't side-stepping be seen as standing on one foot, which pushes you in the direction of your center of mass?

@KaPy3141: Depends on how you do it, of course, and easier to do than describe, but basically you stand on the downhill foot, extend the uphill foot while remaining balanced on the other until the uphill foot is firmly planted, then transfer weight to the uphill foot, and lift the downhill foot to place it close to the other.


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Identify black insect on Granadilla plant in South Africa
Planted a granadilla tree 3 weeks ago and these guys appeared on the new growth.
Never seen them before.

You can use an app like iNaturalist to both make a formal observation for the scientific community, but also to identify organisms with pictures. You'll need to take clear photos, especially of identifying features in order to get accurate suggestions.

See the guidelines at https://biology.stackexchange.com/tags/species-identification/info for species ID questions.

Welcome to Biology.SE! In addition to following @doremi's advice, please click on the species-identification tag for important information about such questions. In particular, please [edit] in size information. Note that this insect has been asked about before on this site, but did not get an answer. Consequently, you should try other resources such as iNaturalist. If you find out, please follow the [answer] guide and post it here. Thanks!


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What percentage of the mass of green plants / algae is carbon?
Wikipedia says that the human body is about 18% carbon, but I can't find any percentage on how much of green plants / leaves or algae is carbon? I assume it varies, so if an example is needed, what percent (by mass) of duckweed or grass is carbon?

Why do you care?  Context helps us to determine whether questions are worth answering.

I was just interested, some questions get stuck in my head when watching documentaries or reading things. If people do not find the question worth answering, I am afraid my reasons will not make it more worthwhile. Sorry.

See table 1 here.

Life form
reprod organn
reprod organmean/sd
rootn
rootmean/sd
leafn
leafmean/sd
stemn
stemmean/sd

Herbaceous plants
83
42.56± 4.57
749
42.45± 5.12
5181
44.73± 3.45
162
42.41± 3.54

Crop
42
42.40± 5.11
56
38.20± 5.23
85
41.32± 3.38
69
43.26± 3.15

Woody plants
57
48.56± 4.07
1392
47.43± 3.94
12 064
47.83± 3.81
3461
48.16± 3.27

Deciduous broad-leaved
17
46.81± 3.93
513
46.59± 3.55
5074
47.25± 3.42
1581
47.69± 2.68

Evergreen broad-leaved
29
49.64± 4.42
520
47.72± 4.14
4490
48.48± 3.86
1212
47.78± 3.58

Conifers
8
48.25± 2.56
252
48.43± 4.16
560
50.25± 3.33
502
50.48± 3.07

Fern

2
43.64± 3.83
98
44.47± 3.33
–
–

Vine
2
45.83± 0.33
38
46.25± 4.46
251
45.74± 4.77
82
46.73± 2.69

Bamboo

23
45.06± 4.28
30
42.98± 5.09
39
49.20± 3.54

All
142
45.01± 5.23
2306
45.64± 4.95
18 124
46.85± 3.98
3754
47.88± 3.49

For an algal estimate, see here:

Carbon is obtained from the post-carbon-capture flow and compressed to 1 MPa for transport and supply to the growth volume (requiring 248 kJ/kg of gas). Carbon uptake efficiency is 79%. The algal biomass productivity is 82.5 t/ha-yr (23.8 g/m2-d) with an elemental composition consisting of 48% carbon, 6.3% nitrogen, and 0.6% phosphorus (Huntley et al., 2015).

I guess it's not a coincidence that it hovers around 45%, since cellulose is 44% carbon? :) C6H10O5: (612.0)/(612.0+101.0+516.0)=0.44

I guess the issue then becomes how much is cellulose!

I could not find easily understood numbers on algae? The table was great for anything else, thank you!!

@HenryStone see edit pulling a direct quote

@Maximillian Press Thank you for an absolutely excellent answer!


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Can a grasshopper jump with so much force that it could rip its leg off if it was stuck?
I live in Colorado Springs, Colorado, USA and I have noticed something interesting while walking and longboarding the many miles of paths of trails in the city. Grasshoppers seem to get stuck quite frequently in sideway cracks. I see this rather frequently, sometimes multiple times in a single walk, in certain areas, during the day. This alone is not interesting, but I suspect it I suspect that at least one of them may have jumped out of their leg, if you will. I'll explain.
First, I am reasonably sure they are stuck, because I can see them try to get away from me, while one leg remains fixed in the crack. Also, I see countless more (sometimes several dozens in those same areas), that appear to have been stuck, but have since been run over by something (bike, scooter, skateboard, etc.) or stepped on. I see VASTLY more grasshoppers smashed on cracks in the sidewalks, than on the flat surfaces of the paths. I counted a small (maybe 100-200 meters, I admit I am bad at estimating distance) stretch of path and counted over 25 smashed in cracks and only 6 on that flat surfaces. And, obviously, the cracks represent only a small fraction of the total area of pavement. So, as I said, I am reasonably sure they are getting stuck. That being said, it is possible the reason so many grasshoppers get killed in the cracks is due to something else. An example I can think of is that they seek nutrients filled within the cracks. Of course, I am not sure why they would be attracted to the cracks, considering the extreme danger, when they are surrounded by vegetation. Are grasshoppers smart enough to recognize a busy and dangerous pathway through their territory? IDK.
However, if they are getting stuck, could they jump out of their legs? My evidence for that is a lot more sparse. I have only a handful of possible clues. First, I have seen a few (maybe 4 or 5) incidents in which the leg was mangled. In a couple, the leg seemed to be dislocated and nonfunctional; the grasshopper would scurry using its other limbs while the nonfunctional leg was stuck, immobile, in the crack at an odd angle. A couple other times I saw what looked to be a pinkish-white "meat" (maybe coagulated blood?) popping out around where the "hip" was, where the leg connected to the thorax. That was on much bigger grasshoppers (like 4"-6" in length).
Finally, a couple days ago, I was walking again and I looked in a crack and I found what I believe to be a grasshopper leg. I pulled the leg out, and I thought it appeared to be missing the foot, so I guessed it was stuck in the crack. I did not have my phone at the time, so I could not take a picture, and I did not even think to bring it home. I just tried to memorize what it looked like, then when I got home, I looked up grasshopper anatomy and I found this GRASSHOPPERS OF WYOMING AND THE WEST by the University of Wyoming. Judging by that drawing on the leg anatomy, the tarsus (everything from the spur down) was missing.

I never planned on asking a stack question, I just let it go until a friend in California mentioned seeing a grasshopper stuck in a crack in Hacienda Heights, California, USA. I do understand there could be other, good explanations for why a grasshopper's leg was left stuck in a crack, such as predation, but from what I remembered, there was that pinkish-white stuff showing at the coxa, so the predator took it off cleanly at the joint, or at least it seemed. I don't know if it was the coxa or just something protruding out of the trochanter after the coxa was ripped off. Or it could have been something protruding from the coxa, I just remember the end tapering down like that in the picture with the reddish-white stuff coming out.
In order to answer whether or not a grasshopper could jump out of its leg, I believe we need to know two things: 1) the amount of force produced by a grasshopper during a jump; and 2) the breaking strength of a grasshopper leg. The first was rather easy. Now, this does come from a University in the UK, (St. Andrews), but I imagine the grasshoppers in America are somewhat similar regarding the amount of force they can produce. If I am wrong about this, please correct me. The figure it gives is about 30 g (which I believe is grams-force and not the unit of acceleration). I am not sure if this is even the correct figure to use, because I am not sure this is the stress the leg feels, or if this is the right unit of measure for reasons I will explain. Even if this is the right figure, is this enough to break a leg off? What does it take to break off a grasshopper's leg?
Well, that is pretty much the question I need answered. I Googled variations of "breaking strength of grasshopper legs" using different variations and synonyms, and the most relevant of which brought up an NIH National Library of Medicine paper Fracture toughness of locust cuticle. The abstract says,

Our results show that the fracture toughness of cuticle in locust hind legs is 4.12 MPa m(1/2) and decreases with desiccation of the cuticle.

Can someone explain what that measurement is? I type "4.12 MPa m(1/2)" into Google, and this comes up:

Is this the conversion to something? How does this play into the 30 grams force that is possible to be produced to by grasshoppers?
Also of note, I found an article on JSTOR (which frustratingly I cannot read, despite having JPASS) which on the Google search page has the following quote:

The grasshopper's leg muscles are so powerful that at maximum tension they can snap the tendons like threads.

Which is also quoted verbatim here without attribution: How strong are grasshoppers? - About Bugs.
One final thing before I summarize, I realize that if a leg were in a degraded state, such as after several attempts at jumping with a limb stuck in the crack, as well as possibly moving around, twisting it, breaking it more, it would take less force, and how much less would depend on the state of degradation. But, would jumping alone be enough to rip its leg clean off?
Okay, so the questions are:
Can a grasshopper jump with such force that it rips a stuck hindleg off, even after repeated attempts?
In order to answer that I believe knowing the answers to some other questions will help :

How should the force applied to the joints of a grasshopper during a jump be measured?

Is the amount of force produced on the ground during a grasshopper's jump, the same as the amount of force experienced on the legs of the grasshopper?

2a) If the legs experience a different force, what forces do they experience?

What is the measurement of force on the ground in the St. Andrews paper? grams-force, g's, something else?

I found that fracture toughness, mentioned in the NIH abstract is measured in Pascal m^(1/2) (pascal square root meter) not just m(1/2). But is this the measurement needed to determine the breaking strength of the leg. I THINK that would be tensile strength, but that is a wild guess.

Could repeated jumping attempts reduce the leg's strength so much as to be ripped off?

5a) Any idea how many jumps it would take to finally rip it off?
5b) Is a grasshopper capable of this effort?
Any help anyone could give would be awesome. This is something I think about whenever I see these poor creatures grasped by what appears to be death's maws. Kinda breaks my heart a little when I see them. Anyways. Thanks.

4.12 MPa m(1/2) is a textual rendering of $4.12, \text{MPa}, \text{m}^{1/2}$. You can guess it from other units where m(-2) appears, and you can read it properly written in the actual pdf article. MPa is of course megapascal. https://journals.biologists.com/jeb/article/215/9/1502/11309/Fracture-toughness-of-locust-cuticle

Yeah, I figured that out when I put that text in Wolfram Alpha. It made more sense. Thank you for that article.


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What is the effect of anti-fungal soap?
As I understand, most popular anti fungal soap/shampoo has Ketoconazole as an active ingredient. Ketoconazole stops the growth of fungi, but as it does not kill it, but halts division, how can soap/shampoo stop fungal infections? Not all fungus will reproduce at the same time during 5 minutes after soap/shampoo is applied on the skin, so is soap just pseudo medicine?

Ketoconazole is a antifungal drug. How I understand many antifungal drugs, specifically ketoconazole, work, is through inhibition of the sterol biosynthesis pathway which forms ergosterol. Similar to how cholesterol is necessary for the stabilization or regulation of a mammalian lipid membrane, ergosterol works similarly in the cell membranes of fungi. Without ergosterol, it is most likely true that the fungi are incapable of survival.
The sterol biosynthesis pathway is incredibly long and complex, but ketoconazole works specifically to inhibit a key enzyme in the pathway known as CYP51A1. This inhibits the synthesis of ergosterol, as previously noted, which is necessary for most fungi for cell survival - so I do believe that ketoconazole does work to directly kill the fungus. As such, it is an appropriate treatment for fungal infections - the proof of which can be found in the fact that it was clinically approved to do so.

Welcome to Biology.SE. This looks like it could become a good answer, but answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). Without that support, your answer appears to be speculative opinion and is thus inappropriate for this site. This is a good example of how to format references. ——— Please take the [tour] and consult the [help] pages for additional advice on [answer] and [ask] effectively on this site for details.


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What bird species were featured on this album?
I am very curious about the identity of the feathered subjects on the cover for Susumu Yokota's 2000 Album "Sakura."
The one on the left seems to be some kind of hummingbird. Not sure what family the two on the right belong to, let alone genus or species.
Assuming they aren't fictional species created in an ad-hoc manner for the album art, which I hope isn't the case, does anyone recognize them?

There are two species of bird shown in the illustration.  The one on the left is Eupetomena macroura, the swallow-tailed hummingbird.  This bird lives in eastern South America, primarily Brazil.
The species on the right I can't identify.  From the style of the illustration, it appears to be  a 19th-century zoological illustration, and is not likely to be an original for the album cover.

It looks very much like the work of ornithologist John Gould's wife, Elizabeth.

@ mgkrebbs Wonderful. I had a feeling the hummingbird was real. As for the other, perhaps you might be right. It has to be a passeriform at the very least. I find unsolved mysteries rather troublesome so perhaps I'll try to get a definitive answer elsewhere.

@anongoodnurse I looked at her illustrations on Google and the birds she drew bear a striking similarity to these little ones. There's no artist credited for the cover on the album's Wikipedia page or Discogs, so who knows who created it. I don't think it's likely that he had some other artist's work copy/pasted though.

Perhaps Sunbirds of some type?


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Why is the process of releasing gametes in females different from that of males?
In context of humans, males produce sperms, store them (for few weeks? then regeneration?) and ejaculate them "on demand" but females can not do that. Females have an almost fixed pattern of production and release of ova leading to menstruation most of the times (menarche to menopause).
I know release of ovum is accompanied by some additional "preparations" for possible conception.
Why could nature/evolution have not "designed" the reproductive system in females similar to that of males eliminating the need for menstruation?

Production and release of ova during pregnancy could have been regulated (like milk in mammary glands) by hormones to prevent multiple pregnancies.

I guess it has something to do with the time taken to "prepare" the body for possible conception and, production time and survival time limits of ova and sperms.

Each individual optimizes the probability of offspring carrying their genes. Anatomical and behavioral optimization between sexes contribute to distinct strategies used between different sex.

I guess it has something to do with the time taken to "prepare" the body for possible conception and, production time and survival time limits of ova & sperms.

True. This is the hypothesis of any mating cost.
We need to understand two concepts. First, every investment has a cost (of offspring being dead). Second, every individual wants its genes to survive and propagate.
Consider a case of a mammal mating. We currently understand that the embryo will stay inside the womb for longer times inside the female. That means, what are the best chances a female can raise an offspring?

make numerous ovums that has equal chance, or
sacrifice numerous ovum contents, but one to form a single stable ovum?

The latter option would be better, while the former option allows the mammal to rear as much as possible, if the offspring die before birth say 50%, that will cost a whole lot of survival opportunity for the female. The latter is much clearer, we can get an almost good guarantee the offspring will at least be born alive.
Now, comes to a unique part. Since females can only have extraordinarily little amounts of ovums, would accepting weak sperms do the math above? Of course not. That's why some female mammals observe sexual selection, either by copulatory structures or behaviors that could indicate weak and strong males.
However, the need of females to preserve their genes hinders the males' effort to preserve their own. How is that? By selecting males, there would be less chance to fertilize the ovum. Remember, males need topreserve their genes. Which option will give the best chances, considering the females' investment above?

just one sperm, just one mating
copious amount of sperm, multiple mating

Even a single sperm would not be guaranteed entry to the ovum, why should consider the former? The latter would be better. Since females will always raise their offspring, mating multiply and with much more sperm content will increase the chances of the females' offspring will be the males'.
This is just a surface of the evolutionary basics that drive the mating behavior. In fact, both contribution and behavior will drive each other, resulting in complex behaviors such as Lek mating, or even paternal care.
I suggest you to read books about evolution and animal behavior such as Futuyma and Dugatkin. If you want to understand quickly, read Unit III of Futuyma. But try to read it from A to Z, both are great introductory books on the logic and hypothesis of evolution and behavior. After reading those books, you can read more research papers about mating cases you find intriguing. (If you want the quickest takeaway, see the TL; DR)
Good luck!


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How does a stimulus causes a voltage change in nerve cell?
I know about the opening of voltage gated sodium channels and then how the membrane becomes depolarized when the rise of potential greater than threshold occurs.
But what happens initially after the stimulus that causes a change in potential and makes it reach up to the level of threshold?
Like what that light, touch or chemical did?

Ligand-gated ion channels, mainly. Ligands can be neurotransmitters like glutamate or acetylcholine, or extraneous chemicals. TRP channels can also be sensitive to things like temperature. Mechanoreceptors and hair cells in the cochlea used in audition are gated mechanically. Gating can be direct or via a second messenger; photoreceptor cells use a chemical conformation change triggered by photons to detect light, but the actual voltage change comes by a channel gated by cyclic GMP.


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What are these most tiny bugs called
These bugs are the smallest bugs I've ever seen in my life and they are very annoying, throughout the day, I just feel sudden scratches on my body and when I look closely, the cause are these bugs moving on my body, they are making me lose my mind. They are hard to kill, putting pressure when they are between my fingers does not kill them, I need to press them against hard flat surface to kill them. They go inside my laptop, from the keyboard holes and touchpad which could possibly damage it and they are everywhere and there's a lot of them.
Here's an enlarged image of one of them moving on my monitor's screen:

The rest of the images are not zoomed in so you can get a sense of how small they are, please zoom in on them as you wish:

What are these bugs called?
I've been googling a lot, the closest I could come up with was bed bugs and Argas reflexus and they are not either of those.


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Osmotic Pressure and Enzyme Activity
Is it true that in an enzyme-catalyzed reaction, the rate of reaction does not vary with varying osmotic pressure?
Instead of just a true or false answer, why does it, or why does it not vary with osmotic pressure?

This paper is a compelling example of an effect of osmotic pressure on enzyme function. Restriction enzymes are normally very selective in the base sequences of sites at which they cut DNA, but in some conditions they show cutting at off-target sites, called "star activity." "Star activity" increased for some restriction enzymes almost linearly with osmotic pressure generated by a range of non-ionic solutes. Supporting the idea that the higher osmotic pressure was directly responsible, increased hydrostatic pressure reversed the effect of increased osmotic pressure.
Increasing the osmotic pressure is essentially decreasing the chemical activity of the water in the system. So it's not surprising that any enzyme reaction might be affected, particularly if the structures of active sites of enzymes are altered as suggested by the authors of the paper cited above.

In order to achieve initiation of DNA replication in vitro at the E. coli chromosomal origin of replication, Arthur Kornberg's lab had to include polyethylene glycol (PEG) in their reactions.
The proposed mechanism for this enhancement was termed "molecular crowding" which was thought to increase the local concentration of the substrates.
A similar effect has been seen in reactions with T4 DNA ligase. Blunt-ended ligations are more efficient in buffers containing PEG.

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Why does protein have 4 calories per gram?
As I understand it, protien that isn't used for building and repairing the body is inefficiently converted into glucose in the liver (at a rate of roughly 3 grams of protein per gram of glucose produced). Glucose has 4 calories per gram. So does that mean that protien would provide 12 calories of energy if the body could convert it at a 1:1 ratio? If not, Where does the 4 calories per gram number come from?

Did you check, if the conversion ratio is indeed 1:1?

It's not 1:1 it's closer to 3:1

Ultimately, the 4 kcal/g numbers come from calorimetry. That is, scientists take a small amount of glucose or protein, put it in a device which burns the material and figures out how much energy is released. Now, this doesn't account for certain factors which complicate matters, such as the fact that humans excrete waste nitrogen as urea and not fully oxidized nitrogen (as is produced in a bomb calorimeter). As such there's some corrections which are applied to account for those differences. When you do the math, you find that carbohydrates and proteins both have about 4 kcal/g energy. As such, most people these days don't actually bother to do the calorimetry to find the energy content, but instead take the content of carbohydrate/protein/fat/etc. and do the calories-per-gram calculation from there.
Now, you're correct that those numbers (from combustion calorimetry) don't match the number you got from the mass balance in gluconeogenesis. Part of the reason for this is that, like most processes, gluconeogenesis isn't 100% efficient. You get some loss as heat due to steps not being 100% reversible. The nutritional content is intended to be more of an estimate of the once-through energy content. (That is, the amount of energy you'll extract if you go directly from the input into a totally metabolized state.)
But perhaps a more important difference is that the mass/energy balance equations for gluconeogenesis from protein can be more complicated than your simple 3:1 analysis suggests -- there's various offshoots of ATP, NADH, etc. generated going from the raw amino acids to glucose. Each of these carries away some energy, and to get a true energy balance. You also need to account for these alternative offshoots of energy.
Which amino acids you're talking about also makes a difference. Alanine is probably the simplest amino acid to feed into gluconeogenesis. It's transformed at a 2:1 molar ratio, which works out to an approximately 1:1 mass ratio (as expected from the calorimetric ratios). Other amino acids like leucine are ketogenic, meaning that they cannot be converted in gluconeogenesis at all (at least in humans). The differences in how different amino acids metabolize can account for the discrepancy. The 3:1 ratio may refer to a "typical" amino acid distribution, which includes a mix of some 1:1 converted amino acids, some which are only partially converted, and some which aren't converted at all.

Super informative. Just to make sure I understood, you're saying that the calories from the expenditure of the product of gluconeogenesis on one gram of  protien is something less than calories from the expenditure of one gram of carbohydrate, and that that number depends on the amino acids in the protien?

@Hal No, what I'm saying is that the "4 kcal/g" figure is for turning protein into energy, not for turning protein into carbohydrate. When you try to turn protein into carbohydrate, there's a number of other considerations to figure in (inefficiency, side products, different behavior of different amino acids). That's why the two values don't match up.

I remember reading somewhere that only 2 out of the ~20 aminoacids were “glucogenic”; that would make the conversion even more inefficient than your answer suggests. In any case, counting calories for weight loss is only meaningful if you keep the macronutrient ratios constant, I guess. Otherwise it’s Apples to Oranges…?


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Is there a good analogy that illustrates the difference between early DNA sequencing techniques and shotgun sequencing?
My first university biology classes begin in September. In preparation, but increasingly out of curiosity, I've been studying some basic biology. Saying that to say, I know as much about DNA replication as the Khan Academy videos teach.
Presently, I'm reading about the two efforts to sequence the genome. From what I've read, Collins' project used "polymerase catalysis and nucleotide labeling"; whereas, Venter's project used "shotgun sequencing". I didn't know enough to understand the article I read on "shotgun sequencing" and couldn't find one that described the other technique.
I suspect that, in order to comprehend a concise description of the two techniques, I'd need to learn more than I could learn from an answer to this question. That said, it'd still be nice to have a very rough idea of what each process involves and how they differ from each other. A crude analogy to something concrete would be great.

You should read about chain-termination (aka Sanger) sequencing; it was used by both projects. Shotgunning is a technique used to assemble an entire genome out of the many short reads from the sequencer. The private project used whole genome shotgunning whereas the public project used the clone contig approach. This looks like a good read for you: http://www.ncbi.nlm.nih.gov/books/NBK21117/#!po=29.2373

The public effort, led by Collins, relied on a physical map of each chromosome.  Very large pieces of genomic DNA were sub cloned into cloning vectors and used to create genomic libraries in cosmids, BACs and YACs.  The sub clones are ordered using hybridization probes from either known genes, or RFLP genetic markers. In this way a physical map of each chromosome was built up, and then the project would march down the ordered clones, sequencing the sub clones.  If the physical map is good then you have a very good idea of where the sequence comes from.
Shotgun sequencing, in contrast, involves randomly fragmenting the entire genome into small fragments (using sonication, for example), sub cloning those pieces and sequencing everything.
In the first method each base is sequenced a minimal number of times, whereas in the second approach each base ends up being sequenced many times (on average).
For a whole genome, shotgun sequencing requires an excellent computer algorithm to "assemble" the resulting data into overlapping contigs.

What information informs the 'decisions' of the algorithm, and what sort of decisions is it making?

Good answer, though I'm not sure how useful it will be for someone just starting biology ;)

I don't think I have the expertise to compare and contrast the pros and cons of the competing approaches.  Have you read the Wikipedia entry on the Human Genome Sequence? There are many good references there. If you are interested in Venter & Gene Myers' algorithm you may find Michael Ashburner's short book about sequencing the Drosophila genome helpful. That was essentially a dry run for the Human effort, and they developed the tools then.  Matt Ridley's book "Genome" has a good description of the shotgun approach, as I recall.

PCR (polymeraze chain reaction) and shotgun sequencing are two somewhat complimentary approaches to sequencing. In the former case one uses chemical reaction to create multiple copies of the genome of interest, which allows to reduce the error in sequencing this genome. The latter is done by sequencing the data directly, i.e., without any genome multiplication.
PCR is more suitable when we are studying a particular genome or a few genomes, e.g., when sequencing the genome of a particular person or a particular type of organism. However, when some very different genomes are present, the amplification might be very uneven, and in fact introduce additional errors. This is why in some situations one prefers shotgun sequencing, e.g., when studying microbiome, containing many different types of bacteria, archaea, viruses, etc.
Both terms refer to the so-called High-Throughput Sequencing (HTS). You could learn a bit more about sequencing technologies from this popular science article.

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Asymmetric volcano plot
Nearly all volcano plot I've seen tend to be roughly symmetric around the y-axis, with a fairly equal number of up- and down-regulated genes. What are the potential reasons for a volcano plot that is heavily unbalanced (i.e., many more negative fold change genes than positive)?
In my analysis, I have identified two populations of patients within a disease cohort, representing the "interferon high" and "interferon low" sub-populations. I then calculate differential expression between these groups, and visualize the results with a volcano plot (log(p-value) of differential expression vs. log(fold change)). The volcano plot is quite asymmetric, with a maximum log2 fold change of 1 on the positive end, and a minimum log2 fold change of -3 on the negative end, with many more genes significantly down-regulated in the IFN-low population.
Is it reasonable to suppose that there are lots of genes up-regulated in IFN-high, with no down-regulated genes defining this population, or is there something else going on?

I have no experience on mammalian expression analysis but I have seen these asymmetric plots quite a few times when cells were highly stressed. During one treatment they shut down protein biosynthesis and photosynthesis so downregulated genes vastly outnumbered the few genes which were involved in the adaptation response. I don't know if something similar could be happening in your samples?


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Help identifying possible fossil found in coastal northern Iran
This was found in Jangels near by the sea, in North Iran:

can  you add something for scale or give the dimentions and please edit this into your question.

Pictures from the side and bottom would also help. Having said that the term "echinoderm" springs to mind. Which one, I have no idea.


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How do we know that the DNA we share with other species (especially primates) isn't fully the result of transposable elements?
I recently read a couple studies that concluded the 25% of genetic similarity between cows and reptiles is actually primarily due to TEs (transposable elements) rather than common ancestry.
Here's the link to the study for more information: https://www.theatlantic.com/science/archive/2017/10/how-a-quarter-of-the-cow-genome-came-from-reptiles/542868/
Now, I'm a strong believer in evolution, but I'm wondering if there's even the slightest possibility that the 97-99% number floating around when it comes to human and chimp/bonobo genetic similarities isn't exactly accurate, especially with the existence of TEs. I supposed my question is, simply put, could TEs serve as an alternative explanation to common ancestry for humans and modern apes? Also would this undermine the ERV/retrovirus remains argument as well?

Never say never in biology. But it is not plausible that TEs explain the similarity in great apes (including humans).
Much (most?) of the argument for similarity is and has always been due to essentially identical coding sequences, which are mostly not affected by TEs.
More convincingly, the high degree of synteny between great ape genomes (including humans) is extremely unlikely if generated by independent random processes. For example, there is only one major difference in the gross ordering of elements on the chromosomes between humans and chimps.
The bovine/reptile similarity from TEs is mostly noticeable because it's on a background of quite low similarity at the coding level, and essentially no similarity at the synteny level. The BovB element is <20% of the cow genome. I don't know of high-level similarity numbers for the overall genomes of those organisms because I don't think the genomes are even alignable enough to compute those statistics, but I imagine they are quite low.

Thank you for your answer! Is it likely that TEs could at least be used to explain away the same ERV remains in human/primate genomes or is even that unlikely?

@MihirDhawan since you seem to be new to the Stack Exchange network, please read What should I do when someone answers my question? in the [help].

@MihirDhawan Certainly, humans and great apes are quite closely related so they have quite similar TE profiles, both active and defunct. Perhaps I am not understanding the question? In other words, they share TEs rather trivially through common descent, rather than through horizontal transmission (which is what makes that bovine case interesting). If what you are asking is "does horizontal TE transfer occur between apes and humans?", then that should probably be a separate question, as it's a bit different in scope.

@MaximilianPress Yes, I think that's what I'm trying to ask--does horizontal TE transfer happen between apes and humans. Thanks again, I'll post it as a new question!


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How would one model a Neutrophil Extracellular Trap with Hookean Springs?
This is a question based in biology but involves a good amount of physics.
Given that a Neutrophil Extracellular Trap (N.E.T) behaves like an aggregate of DNA strands with citrullinated Histones and defensins such as Myeloperoxidase and Neutrophil Elastase, and that DNA itself can be modeled as a Hookean spring (maybe with a variable spring "constant"), I thought that it would be possible to model say a 100 uM X 100 uM Neutrophil Extracellular trap as a network of hookean springs.
I think that this would require one to ascertain the length of the DNA strands incorporated into the N.E.T as well as the configuration of these many strands. The configuration will determine whether the spring constants of each DNA strand are additive (for parallel springs).
Is there some approximation of configuration and DNA length I could use to maybe get one cumulative spring constant for a N.E.T of a given size or is more complex notation required? Also the purpose of my asking this question and even modeling a N.E.T as a network of springs is to gauge the compliance and compressive stress that can be generated by the N.E.T.


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If you add type A blood to type B blood, is there a visible reaction?
I read that the original discovery of blood types was because they combined random blood samples togethers and noticed a reaction. I was wondering if this was a visible reaction? Or is anti-A or anti-B serum explicitly required?

Blood contains serum too.


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Did snow leopards lose the ability to roar or never have it?
Since snow leopards are the only species in the genus Panthera that can't roar, was this something the others developed after snow leopards diverged or something that snow leopards lost?

Interesting topic. I found a recording of all the Panthera clade roars here, and comments like "roaring and purring are mutually excusive" and " Its vocal cords lack an all-important layer of fatty, elasticated tissue, which, in other big cats, gives the vocalisations an uneven rumble that emerges as a roar" but no information to answer your query, which is very specialized zoology/big cats info.

https://www.youtube.com/watch?v=bFCv02IGtn4&ab_channel=MeowMeowTV


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Are there animal species with sex of an offspring determined by sex of preceding offspring?
For instance, if an animal's first offspring is male, then all subsequent offsprings will be male too (the sex of first offspring could be determined randomly).
Does it happen in any species?

Are you interested in processes operating both pre- and post zygotic formation, and both pre- and post ovulation? In other words, are you asking only about primary sex (primary sex ratio) or offspring sex at birth. It is also possible to have a situation where parents adjust sex ratio of offspring at the egg stage (e.g. birds) or when offspring are very young (e.g. by adjusting feeding rates), and this could theoretically be influenced by the sex of previous offspring.

I mean sex ratio at birth.

fileunderwater, what you mention would be tertiary sex ratio. It's adjustment is also an interesting question, but I wonder if there are any physiological mechanisms that can adjust secondary sex ratio depending on the sex of preceding sibling. We don't know if such mechanisms exist in humans, but perhaps there are animals with a known effect...

I can think of one (perhaps trivial) case where this happens. In insects with haplodiploid sex determination (like Hymenoptera) then almost all of a male's offspring will be female, as they will be diploid.

Another case you might think about is female-only, clonal animals, e.g. https://www.nytimes.com/2018/02/05/science/mutant-crayfish-clones-europe.html

Why 'almost' all?

Also I'm not sure this answers the question, as the sex of offspring 2...n doesn't depend at all on the sex of offspring 1.

Regarding "almost all," in bees, for example, sex detemination occurs at a single genetic locus. The usual rule is hemi- or homo-zygous for the sex determination locus, you're male, heterozygous, you're female. So in inbred populations diploid males are somewhat common, in outbred populations they're very rare.

And I agree, neither of these cases is as weird as the OP asks about, where the sex of first offspring might not be predetermined, but has a large effect on the sex of subsequent offspring. I am sure if you look long enough you'll find a story that matches it; I thought it might be helpful to share some more common stories that might be food for thought.


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Is this a sentry palm?
I "inherited" a plant and was trying to identify it (to understand how to take care of it - plants usually have a hard time with me).
I belive this is a sentry palm (from photo matches gathered on Internet) but my leaves seem much more narrow than the ones on the pictures.
The plant is in France and is probably not a fancy one (in the sense that it should probably be available in Ikea or a general plant store).

Note: this question should be made to gardening.stackexchange.com

@GiacomoCatenazzi: I had no idea that such a site existed (I will have to look again at the new members of the network). Yes, that would have definitely been a better place.


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Why don't bees sting hornets for defense?
Why don't honeybees sting hornets for defense when their hive is attacked? It seems like a good weapon against bigger animals - why not against hornets?

Can you provide a reference showing that they don't sting hornets?

@MattDMo I watched youtube video of japanese bees using heat to kill hornet but not sting.

Smithsonian mag says that the bee stings can't penetrate through the predator hornet's armor, which is simply a case of the hornet's armor being tougher than the blunt barb of the bee sting. https://www.smithsonianmag.com/smart-news/invasion-murder-hornets-180974809/
Here's a good research:"

To examine their behaviors of penetrating into different materials, we performed penetration–extraction tests and slow motion analyses of their insertion process. In comparison, the barbed stings of honey bees are relatively difficult to be withdrawn from fibrous tissues (e.g. skin), while the removal of paper wasp stings is easier due to their different structures and insertion skills. The similarities and differences of the two kinds of stings are summarized on the basis of the experiments and observations.

Some research suggests that bee stings have evolved to ward off vertebrates, physically and chemically. Wasps have more slender stings and perhaps that's why the hornets prefer bees nests.
Actually, a lot of insects have phenomenally hard keratin, beetles and the bulldog raspy cricket, as far as i know, even parasitoid wasps which have specialized stings evolved to cope specificially with insects are more common on caterpillars and spiders than strongly armored animals like big beetles.

Keratin or chitin? Insects have chitin exoskeletons.


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Why is decomposition process much slower for poisoned insects?
I have always noticed that the pest roaches killed by roach spray start to break down much more slowly than a roach that was stomped or attack by a lizard. In those cases the roach's body attracts ants within an hour or two, and they leave the wings and antennas after a couple of hours or so.
But when I kill a roach with spray, there's no ants or flies. The antennas break after 24 hours but the body stays intact for at least a week, provided that the roach is kept in a clean and dry place but has access to air.
So, if there's no maggots or attracted insects because of the poison, the only decomposition happening is from the bacteria/protozoa inside the roach's body? And the cellular death? Absolutely nothing intruding from the outside?

You're wondering why if you kill an insect with an insecticide spray, why other insects don't attack the body for food?

@mgkrebbs No. I was wondering what's happening inside the body and in microscopic level because in non-poisonous cases ants or maggots do the job quickly in front of our eyes. Also, most poisoned roaches go to dustbin before I can get my hands on them, but right now I have a specimen lying on my floor for 7 days straight, visibly unaffected from outside.

Features of a rotting insect carcass
What you see after an insect dies is its chitinous exoskeleton. It is a tough biomaterial that takes time to decompose, given its structure, and few microbes can digest it, let alone as quickly as soft tissue. It's a little bit like human bones. The insect's inner soft parts will degrade quickly, just as with any dead, soft tissue. However, what remains looks intact, because the outer cuticle is resistant to deformation; it keeps its shape!
Exoskeleton decomposition by insects
Ants are known to, and can and will break exoskeletons into pieces and carry it away in parts. They are ubiquitous and exist everywhere, so it's no surprise you see them doing this job all over the place. Flies and worms and mites may also feed on the softer parts and on the yeast or microbes that flourish in the decomposing tissue. It is also possible that some insects lay their eggs into the carcass, which would in some cases be a rich source of nutrition for the young insects, when they are in their larval stages (what you may confuse for worms).
Poison deters exoskeleton decomposition by other insects
If you introduce poison into the mix, obviously the roach carcass with be contaminated and its exoskeleton will remain relatively less likely to be touched by other insects, since it remains noxious to them. The effect on micro-organisms would be less pronounced, but that depends entirely on the contents, concentration, volatility and weatherablity of the insecticide that was used.


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Alleles and Ploidy
I was recently studying inheritance and variation and came across a sentence:

A diploid organism can show only two alleles

How is this possible?

@Andrew Thanks I got it. Should I need to delete this question. Or leave it as it is

"In a diploid organism, one that has two copies of each chromosome, two alleles make up the individual's genotype."

Source

Human is a diploid organism. We have 23 chromosomes. Every body cell has 46 chromosomes, one set of 23 chromosomes from mom another set of 23 chromosomes from dad. There is one chromosome number 1 from dad another chromosome number 1 from mom. Each chromosome contains in average 1000 genes. Each gene encodes a protein. For example half of the hemoglobin (the protein of red blood cells that transports oxygen) is encoded by the gene that you had from your mom, the other half of the hemoglobin is encoded by the gene that you got from your dad. In both cases you are encoding the hemoglobin, but the exact structure of the molecule can be different. These differences are representing the allele. The idea is generalized to all other 20'000 genes of the human genome encoding other proteins (such as insulin, hair, skin, retina proteins).
There are slight exceptions to everything I said which you can ignore at this stage (for example some cells do not have chromosomes, because they destroy them, and reproductive cells have only 23 chromosomes instead of 46).
Hope that this helps


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What is the evolutionary advantage of breathing and heart beats syncing between partners?
I recently read that partners who are close to one another usually when touching have their heart beats and breathing in sync. Why does this occur? What is the benefit of it occurring? How does this occur?
The study linked below states that this phenomenon may reduce pain. Is it possible that is the evolutionary advantage? How is it that 2 peoples bodies sync their heart rates without knowing the other persons heart rate or being able to see the other persons heart beat?
Goldstein, Pavel, Irit Weissman-Fogel, and Simone G. Shamay-Tsoory. "The role of touch in regulating inter-partner physiological coupling during empathy for pain." Scientific reports 7.1 (2017): 1-12. APA

I think you need to make your question a bit more focussed. The proximal reason (how - i.e. the causal physiological mechanism) is very different to the ultimate reason (the 'evolutionary advantage') - but you seem to have asked both. I suspect that the former question could be answered - but question involving the 'evolutionary reasons' of such a trait are often impossible to answer without speculating, since we can't go back in time to investigate the different selection pressures which may have driven it.

That's a pretty weird study. If you had posted graphs from the study it would be a much better question. The graphs that they researchers drew do not demonstrate very amazing measurements at all.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6421336/


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Telling distance with one eye
Basic mathematical/logical reasoning makes it clear that you need two eyes to have depth of vision. By seeing an object from two perspectives, our brain can calculate the distance of the object based on the angle from each eye to the object. However even when I close one eye, I am able to judge reasonably well the depth of objects. Furthermore when I look at a picture I can instantly (I tried to be as unbiased as I could about this) tell it was a picture. How are we able to do this?

Not a real problem, but I was confused about "when I look at a picture I can instantly ...tell it was not a picture". Which one did you mean?

@VolkerSiegel Oops! That made no sense. My bad. Fixed.

Depth perception consists of what are called monocular cues and binocular cues. As you mention, binocular vision has a lot of advantages for depth perception, but it is not completely necessary.
Many animals, particularly those that don't need especially precise vision, have little to no binocular vision, opting instead for visual coverage in more directions by having eyes on the side of the head.
The Wikipedia page I linked at the beginning has a whole list of various monocular cues, but I will mention a few of them here as well that I think roughly outline the different "categories" of monocular cues.
Relative size is a simple one: you expect certain objects to be a certain size. You can use that information to approximate distance.
Motion parallax: moving relative to objects gives you more information. Nearby objects move very quickly across the eye when you move, far away objects do not.
Accommodation: when you focus on a nearby object, you can estimate the depth by how much the lens needs to be deformed to bring the object in focus. The brain gets a copy of that muscle signal that it can use to estimate distance for nearby objects.
Although monocular depth perception is actually quite good out in the natural world, it is possible to trick the system with sufficiently clever strategies, like many other types of optical illusions. The Ames room is one of these.

Thanks! Its pretty fascinating how we have so many backup algorithms built in.

If we couldn't do this stuff, a lot of 3d graphics and video would be hard too :>

May I recommend an added link to the Ames room?  Wikipedia has a great page including a video link showing just how easy it is to fool our monocular depth perception.

@CortAmmon Done. Although I disagree with you about "just how easy": that's a pretty specially created circumstance. It's remarkable because of how well it breaks a system that 99% of the time does quite well.

that's amazing I had the same question and know I get it in brief I know one factor can be accommodation but don't think of other factors ,I am in high school and most things here I don't get but hopefully I will be able to understand them later . if I do MBBS will they teach this stuff to me?


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Infinite site model and Watterson's Estimator
Why is it that under migration, the watterson's estimator (theta) is upward biased? What does upward bias means? And why do we have downward bias under exponential growth? Lastly, is it only the watterson's estimator whose variance would decrease with increasing recombination rate or would the tajima's estimator's variance would decrease too?


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Why aren't drugs tested on sick patients proactively?
I read an article about a new drug which may stop neurodegenerative activity in the brain and this triggered a question I had for some time already.
Why such novel drugs are not tested on seriously/terminally ill patients, to check whether they are not dangerous, and maybe useful?
I completely understand the need for double - blind trials which can assess that the drug works or not. This requires a lot of tests beforehand to make sure that the drug is reasonably safe for humans.
On the other hand I am sure that seriously or terminally ill patients would take the risk to, maybe, have a chance with the new drug, with the risk of complications (all in reasonable boundaries). I know I would.
Beside some indication that the drug works or not (again, I understand the  implications of a lack of double-blind trial but if the result is 100% success or failure, it is at least one data point) it could be an indication of its lack of safety. If all patients develop an unrelated organ failure (as it was the case in the article I linked), it would help research which otherwise relies on similarities between animals and humans.
Is it just an ethical concern or are there scientific reasons not to use these opportunities?

For one reason: It is extremely unethical. Additionally, such patients are not really the optimal candidates, as they have underlying diseases and treatments, which might affect the outcome of the trial without anybody noticing. Then you want to have a homogenous treatment group to detect negative effects of your treatment. There are some examples of new drugs being tested in patients, but these are then the last hope to get some treatment.

Sometimes they are, as mentioned by Chris. But keep in mind, please, that without proper testing (and even sometimes with), drugs may shorten a lifespan. There is an ethical and scientific responsibility to avoid administering drugs willy-nilly, just because someone is close to death. With trazadone, there should be ample evidence out there already, visible through the retrospectoscope. Many drugs have found a new use through this method, including minoxidil and amantadine.


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What insect is in the PHP bugs logo?
Well, maybe this is a question more suited to Stack Overflow, but anyway, I am curious, which insect is the one in the logo of the PHP bugs site? Is it an actual insect or just a generic "bug"?

It seems like some kind of Hemiptera for me, probably some kind of "true bug". A quick google search about these insects and I found the Hemiptera suborder Heteroptera, and this critter is probably from this group.
I tried to search by the image in google images, but only found the logo itself, in the same low resolution is the image above (I was not able to find a better version of it). I tried to remove the background from the image then, but still I didn't get any photo of the possible species of this logo.
EDIT: this was the PHP bugs logo up until 24th July 2017; the next day it was changed to another different "bug". This question is about the former logo, not the current one.

It is an actual insect, Lethocerus americanus, also known as Giant Water Bug. See:

Matches the colors, body shape and small eyes and head. And yes, they are very annoying. As expected from real bugs. You know, like the first one.

Most probably it is Boxelder bug, since their other logo clearly depicts it as seen here
As per wikipedia

The boxelder bug (Boisea trivittata) is a North American species of true bug.
  Trivittata is from the Latin tri (three) + vittata (banded).
  Their congregation habits and excreta can annoy people; for this reason, they are considered nuisance pests.

Really, this bug is pretty similar to the one in my logo; the only difference I am seeing is the red coloration, but this can be a graphic design adjust for the logo; unhappily I was not able to find a better resolution version of that logo to compare the details...

Very light orange like coloration can be seen at back of insect in that logo too. Se their other logo which  clearly shows that insect

yes, you are right, in the other logo the coloration is pretty clear; I'll wait a bit if another answer comes, but I think this is the correct one. Thanks!


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Where can I find FDist2 executable?
I am trying to download the program FDist2 (Beaumont and Nichols 1996) for Mac but for some reason it appears that all the links I find are broken.
It appears that the program Lositan is an faster implementation of FDist2 but in my understanding Lositan works only through a GUI and not via the command line (and given the number of analyses I want to perform I need to be able to run this algorithm from the command line).

I found this link in Mark Beaumont's web site. The links seem to work. I am not completely sure whether this is a question for this forum though.

Lotterhos and Whitlock 2014 recoded fdist2 in R and it can be found here on Dryad.

The link that ddiez has mentioned, has a download link for a zip file (fidist2). The zip file contains windows executables and C-codes. Just compile the C-codes in your terminal.
This is from the readme:

The .exe files are pc binaries, which is only what most people want. I
  include the source file in case anyone wants to play with them. In
  this case compilation is e.g.:
gcc -o fdist2 -O fdist2.c -lm
gcc -o cplot -O cplot.c as100.c as99.c -lm
gcc -o datacal -O datacal.c -lm

Actually in the readme, the first compile command says fdist.c (no such file) instead of fdist2.c. I corrected that here.
Your system should have gcc. I tried compiling in my system (linux) and it works. It should work in Mac too.

OS X doesn't come with a compiler by default, but if you install XCode and the command-line tools, you'll get clang, which works (in this case) very much in the same manner.

@MattDMo ohh okay.. I didn't know that... That's bad .. This page says that XCode comes with gcc (don't know what version but once you have a compiler you can always compile the other versions).

Well, I'm avoiding a lot of "nerd" details. I think the command gcc will work from the command line once the proper tools are installed (@Remi.b, make sure you run XCode first!). The problem I'm running into currently is that the files aren't compiling. Remi will need to find a C expert, I think....

Yes, the compilation fails on Mac. I'll try to figure this out (eventually with some help from the StackOverflow community) and suggest an edit. Thank you!

@Remi.b Have a look at this page.. Once you compile gcc on your system, you won't have much trouble. Having gcc in your system would be useful for other purposes in future as well.


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Behavior of plant guard cells: open or closed stomata
On an exam of mine, I had the following question:

The interaction between the guard cells and stomata in a plant leaf can be seen in the diagram below.

In which scenario could the guard cells and stomata be in situation 2?
(A) High humidity
(B) High light intensity
(C) Low temperatures
(D) Nighttime

The answer choices aside, I was thinking the answer should be along the lines of "a scenario in which the temperature is really hot", since an open stomata on a very hot day would cause a plant to lose a lot of water. The only answer choice that seems to fit this is "high light intensity" (although I'm not sure if high light intensity would necessarily cause high temperatures, but this seems to be the closest thing to what I predicted). However, the exam key is saying that "D", nighttime, is the correct answer. My teacher explained that since plants don't need to do the light reactions during the night, they apparently close their stomata because they don't need to intake CO2. But this doesn't make sense to me: why would a plant close its stomata during the night instead of keeping it open to stockpile CO2 for use in the day? If I'm not mistaken, this is precisely what CAM plants do (although there's no mention of whether the plant in question is a CAM plant).

I found a paper and this is the link https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258058/  it says that Stomatal opening is induced by low CO2 concentrations, high light intensity and high humidity. By contrast, closing is promoted by high CO2 concentrations, darkness, drought and the plant hormone ABA.
Another paper, Open or Close the Gate – Stomata Action Under the Control of Phytohormones in Drought Stress Conditions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652521/
During the night, elevated levels of CO2 in the leaves were observed due to respiration. It has been proved that CO2 has a positive effect on the stomatal closure process


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Resting membrane potential: K+ concentrations and charges on inside and outside of the neuron
According to this site, there is a greater concentration of K+ ions inside the cell than outside. The following screenshot, taken from this website, supports this statement.

However, I don't understand how the inside of the cell can have a net negative charge if there is a greater concentration of K+ inside the cell. This seems like a contradictory statement to me. (1) Why is the interior negative despite the fact that there are more K+ ions inside than outside, and (2) What exactly causes the net negative charge?

Why is the interior negative despite the fact that there are more K+ ions inside than outside, and (2) What exactly causes the net negative charge?

It's because K+ isn't the only player in the game. Yes, there is a bigger concentration of K+ inside of the cell, however, there is also a higher concentration of Na+ outside of the cell, and also, there are other charged ions, such as Cl- or proteins.
One of the main reasons for the gradient is Na+/K+ ATPase, which transports 2 K+ ions to the inside of the cell, while 3 Na+ ions are pumped to the exterior of the cell. This generally yields in a higher concentration of + charge on the outside of the cell.
The final membrane potential depends on the permeability of the membrane to these ions. Higher the permeability for an ion, the closer is the actual potential to the equilibrium potential of this ion. (you can read about its calculation here.). Since the membrane in a normal state is not permeable to Na+ to a big extent, but is permeable to K+, the resting potential is similar to the equilibrium potential for K+, which is negative (the actual value depends on the specific cell type, generally we can say -70mV in neurons). (The K+ is driven to exit the cell because of the chemical and electrical gradient, which results in negative charge inside of the cell). The approximation of final potential can be calculated by using Goldman equation.
The principle is therefore in selective opening and closing of specific ion channels and functioning of transmembrane pumps.

Thanks for the response. I'm still having trouble understanding how the membrane potential can be negative, since the Na/K ATPase is constantly pumping K+ ions back into the cell.

Because Na/K ATPase throws out 3 Na+ for taking 2 K+ inside i.e. +3 outside and +2 inside. Also K+ can move in and out easily i.e. concentration of K+ outside is still more. Adding it with Cl- and other anions (inside), there becomes more +ve charge outside i.e. more -ve charge inside (relatively, if thats what you couldn't get).

Sorry that I'm struggling so much with this. @aayushsrivastav You said that "concentration of K+ outside is still more", but the sources I mentioned say the opposite--that the concentration of K+ inside is higher. Could you please clarify?

K+ is pumped in by ATPase, exchanging it with Na+. But K+ can still move out easily as membrane is permeable to it. Sorry I didnt mean "more outside" I just meant that "as soon as K+ is pumped in, its concentration increases inside. So it moves out creating concentration balance on both sides. So charge inside is (K+ - Na+) and that outside is (K+ +Na+)

Another quick thing to point out is that voltage is a relative measure. Recall that the outside is the "ground" or point where voltage is consider zero. Thus all measures of voltage are relative to this. Excuse my math but lets consider the Nernst equation
$$\frac{RT}{Fz}\ln(\frac{[Ion]_{out}}{[Ion]_{in}})$$
Where $R$ is the gas constant, $T$ is temperature in kelvin, $F$ is Farady's constant and $z$ is the charge of the ion.
Now because we have (arbitrarily) decided that outside is the reference point the outside Ion Concentration is on top. Thus In potassium's case $z= +1$ it is $\frac{[Ion]_{out}}{[Ion_{in}}=\frac{smaller}{larger}$ is a number less than 1. Recall the natural log of a number less then 1 is negative thus Potassium presence on the inside means the driving potential is negative on the inside.
Now take into account what Matej Pribis said, Potassium is more permeable at rest, thus its driving potential is more contributory to the rest state than say sodium which has a lower permeability at rest.
This means at rest the potassium Ions negative driving potential is more contributory at the neurons resting state.

I'd actually like to answer my own question for any future viewers, as I found this exceptional website that thoroughly and clearly explains how membrane potential is established. Then, this page in particular, belonging to the same site, goes into more detail as to how the membrane potential for a neuron is maintained via the Na/K Pump. Thank you to everyone who posted a response!


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Can certain jellyfish photosynthesize in the medusa stage?
Can jellyfish (at least some of them) do photosynthesis in the symbiosis with zooxanthellae in their medusa form as well? I've heard that only Cassiopea andromeda can but I wasn't able to find a credible source upholding such claim. (Wikipedia would be enough)

''Can jellyfish photosynthesize when mature?''
or
''Can jellyfish (at least some of them) in their medusa do photosynthesis? ''
Which one is your primary question?

I'd like to know about the photosynthesis in the medusa form

Then please change the title accordingly. However I think it would get closed as an under researched homework question . I did a simple google search and found numerous websites and a few books claiming that they cannot but their symbiont zooxanthallae can.Take a look at this wikipedia article.I learned something new, so thank you.

@SanjuktaGhosh Of course, I did mean their symbiant

@SanjuktaGhosh The title has no problems. It's common and acceptable to have a broader title with more specific details in the body of the question. Don't be so picky


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What is this yellow-pink flower?
Found in Pennsylvania, Philadelphia County
This is intentionally planted, not sure if it is indigenous to this region. Thank you for your expertise!

It resembles Lantana Camara, from the family of Verbenaceae that is native to American tropics according to Wikipedia.
They come in variety of different colors, and the one you have photographed is the Pink Caprice.

Image Source: Cindy Dyer's Blog

Glad I could help :)


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Using anatomical terms for human organs and parts of plants
I know how to apply anatomical directional terms (e.g., dorsal/ventral, anterior/posterior, etc.) for animals as a whole (bipeds and quadrupeds).
Recently, I've been studying plant physiology, and I came to know that the upper surface of a leaf is the ventral surface and the lower surface of the leaf is the dorsal surface. I cannot understand how these terms are applied to plants and leaves.
I've also seen anatomical directional terms being used for body organs such as the brain.
I want to know how anatomical terms are applied for parts of plants and body organs.

First, for reference, see here for a discussion about the difference in directional terms between bipeds and quadrupeds as well as a fairly complete explanation of word meanings/etymology.

The etymological meanings of the various anatomical directional terms should help explain their usage in body organs. For example:
Ventral -> "belly" side
Dorsal -> "back" side
Anterior -> "before" or "toward the front"
Posterior -> "after" or coming after (opposite to) the anterior

For body organs (or other body parts):
This SE question addresses hands and feet, while this page from Bryn Mawr College directly demonstrates the usage of anatomical positional terms of the brain:

Rostral/ Anterior --->   Head or front end
Caudal/ Posterior --->  Tail or hind end
Dorsal  --->    Back or top side
Ventral --->    Belly or bottom side

Anatomical positional terminology for brains is consistent across organisms. Here is another picture demonstrating anatomical positional terminology of this organ from Santa Monica college:

For plants, see "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):

Dorsal. Pertaining to the back or outward surface of an organ in relation to the axis, as in the lower surface of a leaf; abaxial. Figure 407.
Ventral. Pertaining to the front or inward surface of an organ in relation to the axis, as in the upper surface of a leaf; adaxial. Figure 1428.

Therefore, dorsal/ventral are determined relative to the axis of where the leaf connects to the stem (ie., the axil). Because of this, in my experience terms such as abaxial and adaxial would be preferred when referring to plants.

So, back and bottom are opposite terms. Aren't they?

@MrAP well that depends on which context you're talking about. In some instances (e.g., quadrupeds)  they are opposite and in other instances (e.g., bipedal anatomy) they are orthogonal. In plants, neither appears to be the case b/c from a whole plant perspective, "back" and "bottom" would be synonymous when referring to a leaf. However, just like when we refer to the dorsum of a human foot, using dorsal (i.e., "back") when referring to a leaf uses a different point of reference (POR) than the whole plant -- dorsal still means "back", but in the case of a leaf, the POR is the leaf axil.

This is why word etymology is so important. :p

So, ventral refers to the belly side and dorsal refers to the side opposite to the belly side which is always the back side but ventral may not always be the bottom side. Right?

So, overall, the trick to understanding all of this is threefold. First, understand that each of these words has etymological meaning/background -- e.g., "ventral" originated from terminology referring to the belly side and "dorsal" originated from terminology referring to the "back." The second part of these concepts is understanding that these terms are applied in different fashions (i.e., using different points of reference). Further this is not always done appropriately based on the etymological meaning of the words themselves...

Given all that, sometimes ventral/dorsal are parallel to the ground (i.e., indicating "up"/"down" relative to the ground, respectively ) and other times they are orthogonal (i.e., indicating anterior/posterior). In cases such as the hand (facing palm forward in anatomical position) when the body is supine or plant leaves (point of reference is the leaf axil), the terms ventral/dorsal appear to be backwards (as in dorsal is "down" not "up" relative to the ground). Again, this is because of point of reference. Regardless of changing POR, these terms retain their etymological meaning.

Again, ventral and dorsal should be avoided when talking about plants because in such cases we are extensding these terms beyond their original etymological meaning. Terms such as abaxial and adaxial are more appropriate because they literally directly refer to the plant part that is important: the leaf axil on the stem.