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The falsifiability of natural selection
I was wondering if we could think about experiments to falsify natural selection . According to this wiki : we could invalidate natural selection

“...if it could be shown that selection or environmental pressures do not
  favor the reproductive success of better adapted individuals”.

So, to test this hypothesis we would have to:

Have different individuals that are defined as more or less adapted to a given environment
Put them in that environment
See if the better adapted individuals have a better reproductive success. (I will avoid the word fitness because one can consider it already contains the principle of natural selection)

But is it possible to define a priori that an individual is more or less adapted? Of course, we could suppose a priori that because of some or other trait (higher longevity, higher stress tolerance, or whatever), an individual carrying that trait will be more adapted. But if we find out this individual does not have a better reproductive success in that environment, we could conclude it was just not the right trait to be better adapted and it would not invalidate natural selection.
Isn’t it, on the contrary, the fact that some individuals have a better reproductive success which allows defining them as better adapted a posteriori? There would then be some kind of a vicious circle.
Ok, so one could say that we do not need to define a priori better or less adapted individuals. We could just put individuals in an environment and see if at least some have a better reproductive success. That would mean that they are better adapted –and so that natural selection occurs-. But suppose we find no significant differences in individuals reproductive success: that could indeed mean that natural selection does not exist. But, well, that could also just mean that there was no selection pressure in that environment.
So if we want to test natural selection existence, we need either to get individuals that are a 100% sure better adapted than others; or environmental conditions that 100% sure exert selection pressures on organisms ; and we need to know this a priori. But, it seems to me that considering an individual as “adapted” or an environment as “selective” can only be done a posteriori if we already accept the idea of natural selection.
That’s why, to me, it is difficult to think of an experiment that would falsify natural selection. Is natural selection falsifiable ?

Short comment... Why do you think we have multi resistent bacteria? Let me tell you why... we are selecting those few in a group with higher resistance everytime we expose the group to an antibiotic.

Okay, sorry for that I'll edit my post. Just to be clear however : I never implied that anything sucked and I never doubted about natural selection's validity. This was just a serious question about its epistemological status.

What is natural selection?
Natural Selection (NS) is an evolutionary process causing a directional change in both a phenotypic trait and the allele frequencies associated with particular values of this phenotypic trait whenever there is a trait that

Has a non-zero narrow-sense heritability $h_N^2$

See this post for the definition of heritability
Note that if $h_N^2 ≠ 0$, then it necessarily implies that the trait is variable in the population.

Correlate with fitness variance in the population

See this wikipedia article for the definition of correlation

You may want to have a look at this post (maybe in particular Lewontin's recipe explained in this answer) or have a look at an intro course to evolution such as Understanding Evolution by UC Berkeley if this is unclear to you.
You may also want to have a look at the post How is “selection” best defined?
Note about the environment
Note that the genotype - fitness covariance does not necessarily need to be dependent or correlated with a specific environmental variable. Many selection pressures are indeed independent of the environment. If one specific genotype is associated to heart failure, then the environment may matter little. This genotype will always be associated with lower fitness.
In other words, you do not need environmental change, or environment specific adaptations in mind to test NS.
Would evidence that what is needed for natural selection to happen does not exist falsify NS?
Mutations
I don't think that an evidence that mutations do not occur would falsify NS because while NS needs genetic variation (fuelled by mutations), the process per say does not refer to the creation of new genetic variance via mutations. Showing that mutation do not occur would not per say falsify NS (I think) but it would make the point that NS cannot happen. A bit like, the absence of energy would not falsify the theory of gravity but it would prevents any gravity to ever happen.
The theory of evolution as whole would be falsified if one were to show mutations never occur (or occur at a much lower or much higher rate than currently observed) though.
Heritability
Similarly, if one could show that $h_N^2 = 0$ for all traits (nothing is heritable), then this would also prevent any NS to ever happen
Fitness variance
Similarly, if one could show that there is no fitness variance in population or even that fitness is always independent of the gentic variance (in other words, fitness itself is not heritable), then NS would never happen.
How to falsify natural selection?
You could show that for a phenotypic trait $h_N^2 > 0$ and show that genetic variance correlates with fitness variance (fitness can be measured as the number of offsprings) and yet repeatedly fail to see any change in the phenotypic trait values (or frequency of the loci explaining variance for this trait) over time. Such observations would falsify NS.

I think my difficulty comes from the fact that it is hard to think a situation in which a heritable trait which provides fitness benefits would not bring to a change in genotypic or phenotypic frequency associated to this trait over time. I wonder if theoretical models have shown this possible.

Well, no, I don't think a theoretical model has shown the opposite possible. But it is not because a cause to consequence is too easy to grasp that it makes its formulation unfalsifiable. All our models have been developed following some logical cause-consequence relationships. Some are hard to get an intuition from. NS has the advantage to be a fairly simple mechanism, easy to understand even for a layman.

I also wonder about something you said: can environnent really be independent on the genotype-fitness covariance ? If you put a terrestrial mammal with a heart failure gene and one without it at the bottom of the sea, they'll both have null fitness. Put them both in a futuristic world where every disease is cured before birth, they will have the same positive fitness.

The genotype-fitness covariance is measured on an existing population. You cannot observe the effect of extreme environments not explored by the species range. But I agree this can be misleading. Of course, genotype-fitness covariance would necessarily be dependent upon the environment but not necessarily upon the experienced environment.

@Remi.b This is a good definition, but where in this definition is an ability to distinguish between natural selection and genetic drift?

@Remi.b Depending upon how you define "directional", there can be genetic drift responsible for "a directional change in both a phenotypic trait and the allele frequencies associated with particular values of this phenotypic trait" with the trait having non-zero heritability and being correlated with fitness variance.

@Remi.b Do I not have comment-editing privileges?  To clarify what I mean when I say that there can be genetic drift responsible for a directional change in both a phenotypic trait and the allele frequencies associated with particular values of this phenotypic trait" with the trait having non-zero heritability and being correlated with fitness variance. If you determine that evolution by drift is responsible for a trait (or a modification of the fixated trait), this is consistent with: directional change in both trait & allele, non-zero heritability, and a correlation with fitness variance.

Genetic drift is a stochastic process. So, yes at any given instance the change goes in a certain direction but if you were to replicate the process, then if genetic drift alone is considered, you should have on average no effect on the phenotype and allele frequency.

I don't know why I wasn't notified of this reply.  So, I think what you are saying is that selection comes with an expectation that there is a change in frequency, such that the population is better able to manage the selective pressure in the future than it was before the selection.

The change brought by selection are a change in allele frequency. NS does not necessarily increase the survival probability of the lineage (or whatever you mean by the population is better able to manage the selective pressure in the future).

@Remi.b, why does it not necessarily increase the survival probability of the lineage?  (Hold aside sexual selection and I mean increase the survival probability in comparison to if the selection had not occurred, so hold aside Van Valen's red queen representation.)

I can't answer all your questions in comments (here and on other posts). This last question takes quite a bit of time to address and more text that can fit in a reasonable number of comments anyway. Please ask your questions in new posts.

@Remi.b OK, thank you.  I will ask that question.

@Kjian That is just evidence that NS is the correct interpretation, it is like saying under what conditions gravity could be shown not to be true, the conditions only need to be hypothetical but recognizable and testable. That is the difference between falsifiability and falsification.

@John Yeah that was my question actually - are there testable conditions that could show it not to be true - I don't think it would actually, I was just wondering if such conditions could exist.

@Kjian yes for instance if you could show all population's gene pool never changed across all generations, even if conditions were changed in many many different ways.


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Insects are attracted to light, what if the light is too bright?
Insects are known to approach light sources. I know that they use it as navigation tools, by maintaining a constant angle between their path and the light beam. However, if a light source is exceedingly bright, I mean like "blinding" bright, would an insect still use that as navigation tool?
What I have been thinking is, the insect wouldn't use it, and try to escape from the light source. I believe this because the extreme blindness may cause the insect to damage it's eyes, although I am neither knowledgeable nor capable of confirming this.
Such a thing usually doesn't happen in nature, so I'm unsure if such a test has been made before. Nontheless any help would be great. I also understand that my definition of "bright" isn't well defined, since I don't know the maximum intensity an insect can handle. I also haven't mentioned the insect, so for consistency sake, assume it to be a Black Witch moth (Ascalapha odorata)
tl;dr
Would an insect use a light source that's exceedingly bright to navigate?

Here's a study that addresses methods for pest control using various light parameters. Though it doesn't explicitely state it, the study does say that intensity is used for both attracting and repelling insects that are photoreceptive. https://rd.springer.com/content/pdf/10.1007/s13355-013-0219-x.pdf

"Insects exhibit the following phototactic
behaviors: (A) attraction (i.e., positive phototaxis, moving
toward a light source); this response can be used
to trap pests, but the effective wavelengths and intensities
vary among species and (B) repulsion (i.e., negative phototaxis,
moving away from light); this can be used
to prevent pests from entering a cultivation area by presenting
light at wavelengths and intensities that repel them."

First, your assumption that insects use light as navigation might be wrong, the flight-to-light behaviour is still far from understood. Link. Secondly, I doubt a light can be too bright. The incandescent lights that are often used for trapping them are so bright that human are blinded by them.

source: Stack Exchange

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sort: votes


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Can you help identify this tree from my garden?
The picture is an evergreen tree.
I have seen very similar trees in Northern Italy. I would appreciate any help.

Welcome to Biology.SE! Do you have any idea if this tree is native (have you seen very similar trees around) or do you think the seed / tuber have been imported from elsewhere and planted here?

Can you provide a close up of the leaves/branches? IMO, it's difficult to determine otherwise.

The tree in the picture is growing in dublin, Ireland. Most likely imported ad I have never seen them here before (not an expert) but I have seen what look the same in northern Italy

It's a Juniper, genus Juniperus.
If will feel prickly, and if you run your hand along the branch from the out to the inside it will feel very prickly. If you run your hand in to out, it will be marginally less so, but still uncomfortable,
Crushing the leaves in your fingers will release a sharp, tangy, not unpleasant smell.
Juniper Juniperus communis is native to some parts of in England, Scotland and Wales, and north and west of Ireland, and in fact most of the temperate forest regions https://en.wikipedia.org/wiki/Juniperus_communis#/media/File:Juniperus_communis_range_map.png
The berries are used to flavour gin.
However there are many other species of Juniperus that are often planted as ornamental trees, so it could well be one of these. https://en.wikipedia.org/wiki/Juniper
Best way for a positive ID is take a small bit with you to a large garden centre, or arboretum, and head to the juniper section and compare the look, feel and smell of the specimens.

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

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


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Is there any biological basis for the emphasis on the value of the firstborn son?
Is the firstborn son biologically different in any way from the sons that follow?
Perhaps his epigenome is different? I have heard that a man's testosterone levels decrease when he becomes a father -- could this then have implications for the epigenetics of subsequent sons?

King Joeffrey was a monster. His younger brother, King Tommen, was a sweetie. Jamie is a heartthrob. Tywin somewhat less so (as a dwarf.) So yes, of course sons are different, but not in any predictable way. (Sorry to use fiction to answer, but it's as accurate as anything else on this matter.)

This report from 1 million babies finds a negative effect on health at birth for lower parity offspring: https://cinch.uni-due.de/fileadmin/content/research/workingpaper/1513_CINCH-Series_ardilamolitor.pdf. Whether that is due to biological characteristics of the babies themselves or the mother is not clear.

The firstborn son has equal chances of birth asphyixiation, being born blue, and having negative traits like autism, as the other children, based on the egg-sperm combination. The quality of the gametes of a traditional female mother from age 16 to 30 let's say, does not vary that much.

There are lots of cases reported now that suggest that overall the firstborn child is usually more intelligent. The articles supporting this are based on behavioural and economic study though, so the biological basis is a little lacking.
It's also not clear if this is nature or nurture. The firstborn may benefit from their parents undivided attention disproportionately.
Here's the press release for it. And the coverage from the Independent
and Forbes
I read somewhere that the firstborn is more likely to be overweight too, but I can't find the article now. Other people may know other traits that are supposed to differ between children.

There are apparently downvotes on this. I realise there are non-scientific links but I only provided them for completion. If anyone has a problem with the answer they should provide a constructuve comment with their vote.

It would be more representative of the literature to also report the magnitude of the detected IQ effect, which was roughly 1.5 units in this larger study: http://www.pnas.org/content/112/46/14224.

I expect that 1.5 units probably derives from the cultural effect of competition and favouritism, and the higher likelihood of the the other children to have depression.

I remember reading/hearing something about the effect of older brothers on the chances of people becoming certain types of people.
It went something like the oldest was most likely to be a pilot/doctor/CEO etc.
The second was most likely to be a teacher/middle management etc.
There's plenty of blogs that suggest the more older brothers a man has, the more likely they are to be homosexual. But this obviously doesn't look at whether or not Biological influences lead to this "birth order effect", or cultural influences.
I remember a suggestion that it was to do with antibodies (or some other substance) that builds up in the mother's womb after having son's. But again I can't find any evidence for that, so it might be pure speculation.
NB. I don't subscribe to this theory, but if you're really interested, it might be worth looking at the science behind it.


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What are the causes of abortive initiation?
I was reading more about DNA transcription, and it mentioned abortive initiation. The article gave no explanation as to why the phenomenon occurs.
The only explanation I can think of is that it is an error in the "machinery" of the RNA polymerase.
Is there any scientific research as to why abortive initiation occurs?

What article did you read? Did you read wiki > abortive initiation also?

@Remi.b The Wikipedia article is one of the articles I read. I also read https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2563432/


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How are negligibly senescent animals dealing with senescent cell buildup?
Well known animals like the rougheye rockfish, which can be bought from the fish market, appear to be negligily senecent. Senecent cell buildup appears to play a key role in senecence, in mice at least (http://www.nature.com/nature/journal/v530/n7589/abs/nature16932.html). Is there no buildup of senecent cells in such negligible senescent animals over livetime?


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Purple Mushroom Identification
I found a purple mushroom that looked like this on a nature walk in South Carolina, USA today. This is not my picture, but one that looks exactly like the mushroom I saw. I have searched the internet, but I could not identify it. Does anyone know what this could be?

This Q is too broad: Mushroom identification is very difficult, even with an original picture. The picture you provided is from a relatively rare mushroom. There are much more commen purple mushrooms, like Laccaria amethystina for example.

The image you used is from a Reddit Thread, where the mushroom is identified to be Cortinarius violaceous. More information on Cortinarius violaceous can be found here.
Although it could be a different mushroom, as the picture you provided is not a picture of the specific mushroom you saw.
Another picture of Cortinarius violaceous

Source: velutipes.com
All credit goes to Reddit user tubergibbosum for the identification.


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How are baselines for extinction rates established?
At the time of 2010, the UN Environment Programme estimated that 150-200 species of plant, insect, bird and mammal become extinct every 24 hours, and, that this is nearly 1000 times greater than "natural" rates. (source, para. 5)

My question is: How are baselines for extinction rates (regarding plant & animal species amongst the entire Earth) established, to then be able to say if an extinction rate for a given species is "normal" or not? What factors are considered most relevent?

Good question +1. Note that a species does not have an extinction rate, only a larger clade does (referring to [..] extinction rate for a given species [..]). The accessory question is interesting also and I think deserves its own post. Blending the two questions in the same post make it a bit broad and may discourage some to answer when they can't answer both questions.

@Remi.b I created a new post for the secondary question.. thanks for the advice :)


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At what point in life's history was biodiversity at its greatest?
When considering plant & animal species throughout the entire Earth, at what point in life's history was biodiversity at its greatest?
The aforementioned question stems from this article about extinction rates, and me becoming curious of the period of time where there was the greatest difference between new/current species rates and extinction rates (while favoring new/current species rates).


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How can they know that they found "all the PERVs"? (porcine endogenous retroviruses)
The New York Times article Gene Editing Spurs Hope for Transplanting Pig Organs Into Human links to the recent Science publication Inactivation of porcine endogenous retrovirus in pigs using CRISPR-Cas9
 Niu et al. Science  10 Aug 2017: eaan4187, DOI: 10.1126/science.aan4187.
The highlighted section of the abstract says "...we inactivated all the PERVs in a porcine primary cell line..." where a PERV is a porcine endogenous retrovirus, an RNA virus which carries its own reverse transcriptase molecule and converts to DNA before incorporating into the host's genome.
Question: Do they mean to say all currently known PERVs or is there some way to be absolutely sure that every PERV in the pig's genome is known. In other words, could they have missed one? Could there be an as-yet unidentified PERV? I don't really want to ask about the possibility of an entirely new and unknown class of retroviruses; rather I'm trying to understand how all PERVs as currently defined can be identified in a pig cell line.
The reason that this is important is that the motivation here is to generate pig organs for transplantation into humans. The concern is that the pig genome may contain retroviruses that could then infect the human host, and the further possibility that it could be passed infectiously to others. As pig to human infectious disease is always a concern, starting with a "clean" pig genome is of particular epidemiological importance.
The first sentence of the NYTimes article:

In a striking advance that helps open the door to organ transplants from animals, researchers have created gene-edited piglets cleansed of viruses that might cause disease in humans. (emphasis added)

Abstract of Niu et al. 2017:

Xenotransplantation is a promising strategy to alleviate the shortage of organs for human transplantation. In addition to the concern on pig-to-human immunological compatibility, the risk of cross-species transmission of porcine endogenous retroviruses (PERVs) has impeded the clinical application of this approach. Earlier, we demonstrated the feasibility of inactivating PERV activity in an immortalized pig cell line. Here, we confirmed that PERVs infect human cells, and observed the horizontal transfer of PERVs among human cells. Using CRISPR-Cas9, we inactivated all the PERVs in a porcine primary cell line and generated PERV-inactivated pigs via somatic cell nuclear transfer. Our study highlighted the value of PERV inactivation to prevent cross-species viral transmission and demonstrated the successful production of PERV-inactivated animals to address the safety concern in clinical xenotransplantation. (emphasis added)

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

More intriguing than I realized Sequences derived from ERVs make up at least 8 to 10% of the human and mouse genomes and range from ancient sequences that predate mammalian divergence to elements that are currently still active Mager & Stoye, and "Despite state-of-the-art genomic tools available for retroviral discovery and the large number of retroviral sequences described to date, there are still gaps in understanding retroviral macroevolutionary patterns and host-retrovirus interactions and a lack of a coherent systematic classification particularly for HERVs" Escalera-Zamudio & Greenwood


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Synaptic connectivity in the newborn's brain
In my understanding, learning is related to the strengthening and weakening of synaptic connections. Very roughly said: Synaptic connections that are used often are strengthened, those that are used rarely are weakened. This is basically the Hebb rule.
Assumed that the Hebb rule holds at least partially (of course, there are other factors at work during learning), I wonder if in a newborn's brain the areas where learning will take place are equally weakly connected by synapses (so the pathways will be "built up") or are equally strongly (maximally) connected (so the pathways will be "carved out") or something inbetween. Or are there areas of both/all kinds?
(I assume that there is a maximal connection strength beyond which no further strengthening takes place.)

This is a really interesting question, but I honestly don't think anyone can answer it yet. I might be wrong, but the problem is our models (rats, primates etc.) are born at different developmental periods to us, neurologically speaking. So it's a difficult question to answer using available techniques. If you think about a specific brain region of interest, then you might be able to find some developmental papers that will give you a bit more insight.

Thanks for the comment. But don't you - or any of your colleagues - have a feeling how it might be?

A feeling with respect to species and developmental period and brain area.

My gut says that when a synapse forms it will probably be in a middle ground, then can be affected by either "Long-Term Potentiation" (strengthening), or "Long-Term Depression" (weakening). But there's so many changes going on in a developing brain, that it might be different in different regions. Edit, this feeling is based on when individual synapses form, which happens in different regions at different times (but is likely to be similar cross-species).

If it's a feeling you want, this becomes a primarily opinion based question. I have a feeling that there are strong and weak and as yet non-existant pathways at birth.

All synapses start infinitely weak (I.e, there has to be no synapse before there is a synapse). The degree of development of different brain areas at a given stage of life varies dramatically. I don't think this question is answerable in any general sense but to say something vague like that, without more specificity up front. Voting to close in agreement with @anongoodnurse

I wonder if in a newborn's brain the areas where learning will take place are equally weakly connected by synapses (so the pathways will be "built up") or are equally strongly (maximally) connected (so the pathways will be "carved out") or something inbetween. Or are there areas of both/all kinds?

According to a paper authored by Princeton researcher Deborah Sandoval:

At the time of birth, the human brain consists of roughly 100 billion neurons in the cortex (The University of Maine, 2001). During the early stages of development (between infancy and adolescence), the weight and size of the brain increases significantly (by up to a factor of 5). This increase in density is not contributed to the creation of a large number of new neurons (neurogenesis), but rather an exponential increase in synaptic growth, known as exuberant synaptogenesis (Huttenlocher & Drabholkar, 1998). At infancy, each neuron averages around 2,500 synapses, and at the peak of exuberant synaptogenesis (around 2-3 years of age) the number increases to around 15,000 (The University of Maine, 2001).

..

Shortly after this period of synaptic growth, the network experiences a decline in synaptic density as neuron connections that are used least-often are removed from the network. The process of eliminating/weakening the irrelevant and inefficient synapses during this developmental period is known as synaptic pruning. Synaptic pruning has been viewed as a learning mechanism, where the “pruning” or removal of a synapse is dependent on the neurons’ responses to environmental factors and external stimuli (Craika & Bialystokb, 2006). The processes of synaptogenesis and synaptic pruning in the developmental stages of the brain have been associated with an individual’s “critical period,” a time where an individual is highly receptive to environmental stimuli and, therefore, learning (Drachman, 2005).

Given the claims in those passages, it would seem that learning (for infants) takes place by initially developing an extremely large number of neuronal connections (most likely due to massive information exposure), and then selectively prunes synaptic sites due to a lack of various external stimuli keeping those axons/dendrites/synapses active; the remaining connections are then reinforced (continously excited). So, as you put it, it would seem that the infant brain both "builds up" and "carves out" neuronal connections for the sake of learning.
To further support this idea though, consider the following fMRI images that depict the functional connectivity of an infant's brain for the first year of life. (Function Connectivity of the Infant Human Brain)

Pay special notice to the coloration differences between rows, within a given column, for the infant (first five rows). With dark red being least functional, and bright yellow being most functional, it can easily be seen that, as the infant gets older (is learning), occurrences of yellow tend to form as clusters within regions of red, which indicate locations of highest functional network activity.
If you then continue this pattern and compare the most functional regions belonging to the 12 month infant scan, with that of the adult (bottom-most row), you can see that the concentrated yellow regions in the infant scan become the general (red) functional regions in the adult scan. This only further suggests that those initial, yellow-denoted functional regions (belonging to the infant), matured into the even more dense, functional regions of the adult brain, through the process of pruning unnecessary connections (which creates smaller functional regions), while at the same time increasing signaling strength amongst neighboring neurons (synaptogenesis).
Lastly, to assess the initial strength of each neuronal connection for an infant brain: when looking at the 1-month old scans, it appears that most all regions of the brain have a color that falls within an associated numerical range of .4 to .8, which would suggest that the brain, as a whole, begins at an almost "neutral" state.

I actually think OPs summary of Hebb's rule is more correct than yours. Cells need not be already strongly connected to increase their connectivity under Hebbian plasticity.

I also think this answer is far too rambling and wide reaching to be an appropriate answer on stack exchange; it is not an answer to a specific question, it is a Wikipedia article on neuro development (this is in part why I chose to vote to close the question; it isn't specific enough).

You quoted (part of) Hebb, then wrote a paragraph. That paragraph is your summary. The rambling nature is that you take on Hebbian plasticity, numbers of neurons and synapses, synaptic pruning, excitotoxicity, and molecular mechanisms of synaptic plasticity.

@BryanKrause I've edited my answer to consider your comments. Thanks again.


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Neurons during Numb feeling
We become numb when there is short supply of blood to some parts, as mentioned here.
If that is the reason, why don't neurons and other cells die at that part if they don't receive oxygen and other things needed?

A lower supply of blood does not mean no supply of blood, so my guess is there's generally enough to keep stuff alive for some time. But if the supply is restricted for long periods (think frostbite), then stuff starts to die.
Also, the sensory neuron endings in the skin are normally just one long projection from a cell body, the major components of the neuron are protected by being located in e.g. The Dorsal Root Ganglion.

True, I was thinking more from a frostbite point of view, i.e. stuff will die eventually, but mostly surface tissue rather than neurons etc.

@mgkrebbs I'll remove my comment, as it's a bit misleading. I meant to refer to the article which says "reduced supply of blood to the limbs" implying that blood flow to the limbs is lost, which isn't true.

Simply put, the cells and "other stuff" WOULD die if the blood flow and/or oxygen were too severe, and would be cut off for too long.
It would probably take some time though.

The neurons stop working in lack of blood, why dont other cells stop?

For your response to be better received, please provide supporting information, which may include a quote or two from a reputable source, and/or links to those sources. As it stands, your response comes off as pure speculation, and is too nondescript.

@Charles Is it speculation to say cells will die in the end if blood flow stops? Do I really have to provide sources for this? Now seriously.... as they say, "LOL".... You could as well ask me to prove to you an apple will fall downwards if it detaches itself from the tree.

@Ram Keswani, your question doesn't make sense to me. I don't understand what you are asking. Do you mean to say you believe cells go on living if no oxygen is provided anymore?

@Charles And besides why don't you ask the same thing of user Oliver Houston? He too seems to blindly assume cells don't survive without nourishment.... LOL

@ObiwanKeNoobie Is it speculation to say cells will die in the end if blood flow stops?" -- depending on the amount of time that's lapsed, yes, most definitely that's a speculative statement. Also, when you say "..in the end", are you implying that eventually all cells die without blood supply? If so, then this is a trivial statement to make, since it is so obvious, as you yourself have pointed out. And, since that is the entirely of your response, respectfully speaking, I find your response not helpful.

@ObiwanKeNoobie Sir see, we feel numb because neurons stop working, or work less efficient because of lack of oxyegn. Then the other cells near that area also lack blood and oxygen. If neurons work less efficiently, why don't other cells in that area not work less efficiently or stop working? Or do they work less efficiently and it doesn't matter much?

@ObiwanKeNoobie "and "other stuff" WOULD die .. " what "other stuff"? This is way too general for a scientific community. "It would probably take some time though." -- This statement is extremely, extremely vague and nondescript, supported by absolutely no scientific information. I hope you are starting to see my point..

@ObiwanKeNoobie The entire focus of the OP is on the amount of time that blood flow is restricted from a body region, with respect to any detrimental effects that may occur as a result. That being said, a brief description of the relationship between blood & neurons/other cells in question would first be established, while doing so a time frame of cell death would be established, and then those conclusions would be tied back to the OP to ultimately address & answer their question. This would be an acceptably structured response to this specific question, IMO.

@Charles - "@ObiwanKeNoobie "and "other stuff" WOULD die .. " what "other stuff"? This is way too general for a scientific community." I bet it is. I was merely quoting the asker, that's why I put brackets around it as I found this not very scientific. And you are now pretending it is me ? LOL... I understand you want to be right but please, be fair. It should be clear to you the asker merely edited his question meanwhile, and rest assured I will have to say something about this in the meta talk.

@Charles - "@ObiwanKeNoobie Is it speculation to say cells will die in the end if blood flow stops?" -- depending on the amount of time that's lapsed, yes, most definitely that's a speculative statement. Also, when you say "..in the end", are you implying that eventually all cells die without blood supply? If so, then this is a trivial statement to make, since it is so obvious, as you yourself have pointed out. And, since that is the entirely of your response, respectfully speaking, I find your response not helpful. – Charles 1 hour ago" - Charles my boy as soon as I have the means I am going

... going to report you for pestering me OK? Read again the nonsense you were replying to me. I have other things to do.

Let us continue this discussion in chat.

Sorry, impossible. I can't. I have spent almost the whole day on SE. It will have to wait for another day.


text:
API for gene names by location
Is there any API where I can input chromosome location and it will provide us gene names, for example input chr: 1 location 154714693:154754070 and it will return a list of gene names or ID within this region?

Do you just want the gene names?  BioPython will allow you to subset a Genbank sequence, complete with all the features if you specify a start and end coordinate, but this is only useful if you want more than the name.

With R biomaRt you can retrieve them.

library(biomaRt)
ensembl = useMart("ensembl",dataset="hsapiens_gene_ensembl")
filterlist <- list("1:154714693:154754070","protein_coding")
genes <- getBM(attributes=c('hgnc_symbol', 'chromosome_name',
  'start_position', 'end_position'),
                     filters = c("chromosomal_region","biotype"),values = filterlist, mart = ensembl)
genes
  hgnc_symbol chromosome_name start_position end_position 1
  KCNN3               1      154697455    154870280

Thanks! This is exactly what I was looking for. Can I specify Genome Build GRCh38.p0, Genome Name GRCh38.d1.vd1 in th query? Could you the link for the documentation? I can not find it for how to do more custom query.

Great! The user guide is here, but since there is so much you can do with biomaRt sometimes you'll have to search the web for specific tricks (the code above is partly from scripts from internet and partly from my own scripts). The latest version of biomaRt is using GRCh38.p10, I don't know if that differs much from your versions.

The NCBI as an API called 'E-utilities' (see short intro) that allows access to almost all their databases. It's a bit tricky to get used to it (and sometimes it wants stupid - even discontinued - identifiers as input), but has a lot of power, there are libraries for this in biopython & bioperl (I think), R might have one too. It's possible to exactly the kind of search you want with the 'efetch' method and rettype 'feature table' (or maybe the full xml record) as well as seq start and stop (you need to have the accession of the chromsome one sequence as a qurey ID).
Another thing I have used are genome annotation tables from NCBI. They are on the FTP server (where the structure is apparently in constant flux, so it's again hard to find), but they list all annotations of a given genome assembly and are sorted by position, so you can easily search them with a script - if you are looking for multiple positions this may well be faster then going through an online API (This folder seems to have multiple files, if you want to take a look at it).

You can use the Ensembl REST API. This is how to do overlap queries:
https://rest.ensembl.org/documentation/info/overlap_region
Your example query:
https://rest.ensembl.org/overlap/region/human/1:154714693:154754070?feature=gene;content-type=application/json


text:
What is the definition of an opioid, beyond that it's something that stimulates opioid receptors?
At first glance, this looks like a circular definition.
Is there some way to definitively determine if a given molecule is or is not an opioid? (Medically or scientifically, not legally).
I'm hoping for something more scientific than "if it's on this list, it is; and if it's not, it isn't."
Wikipedia's article Opioid receptor:

Opioid receptors are a group of inhibitory G protein-coupled receptors with opioids as ligands. The endogenous opioids are dynorphins, enkephalins, endorphins, endomorphins and nociceptin. The opioid receptors are ~40% identical to somatostatin receptors (SSTRs). Opioid receptors are distributed widely in the brain, and are also found in the spinal cord and digestive tract. (emphasis added)

Wikipedia's article on Opioid:

Opioids are substances that act on opioid receptors to produce morphine-like effects. Medically they are primarily used for pain relief, including anesthesia. Other medical uses include suppression of diarrhea, treating addiction, reversing opioid overdose, suppressing cough, and suppressing opioid induced constipation. Extremely strong opioids are approved only for veterinary use such as immobilizing large mammals. Opioids are also frequently used non-medically for their euphoric effects or to prevent withdrawal. (emphasis added)

The common-sense answer (also given on googling) is: "Opioids are drugs that are either derived from opiates (drugs created directly from opium, such as morphine or codeine) or are chemically related to opiates or opium."

@anongoodnurse thanks, but that just pushes everything under a rug called "chemically related" which is nearly useless. It is a subjective and fluid concept; there is no litmus test for chemically relatedness. There is no common-sense here, just further ambiguity.

It's not "nearly useless" just because it breaks your question. Of course there is a definition for "chemically related". Look at PubChem or ChemIDPlus to see the structure opioids have in common.

@anongoodnurse given molecule X and Y where X is an existing synthetic opioid, and Y is a completely different synthetic opioid, is there a test, with a binary result Yes or No to the question "Is X chemically related to Y?" This needs to be a test that anyone can apply and receive the same answer in all cases. "Chemically related" is a fluid and ambiguous concept, and is not a scientifically well-defined test.

"...Y is a completely different synthetic opioid..." If it was completely different, it would not be an opioid. It might be an analgesic, or a euphoric agent, or an emetic, but it would not be an opioid. I think instead of arguing from opinion, it would help if you gave an example of two molecules classified as opioids that were completely different in structure. Again, I refer you to PubChem, which will give you the chemical structure in all three dimentions of every opioid.

@anongoodnurse Are you sure? Can you express that in clear, unambiguous terms that can be objectively applied by a third party?  What does "completely different" mean? I think if we continue this we will go in semantic circles. In the end you often end up posting excellent answers to my questions, so I'm happy to go along, but it might not be so interesting to others.

You're the one doing the dancing (semantically); I'm standing in the same position. I'm done here.

@anongoodnurse A PubChem list of every opioid was anticipated by my sentence I'm hoping for something more scientific than "if it's on this list, it is; and if it's not, it isn't." I wonder if there is at least a much shorter list of opioid receptors? So any molecule which interacts with those receptors could be classified as an opioid? At least that approach could be codified with some sort of standard procedure and interpretation of result.

I suspect opioid was originally defined to be chemicals derived opium. Then, when the receptors that these chemicals acted on were identified, other molecules were found that also interacted with them. Thus the Wikipedia definition of opioid receptor may be changed to: a group of inhibitory G protein-coupled receptors which have for ligands chemicals derived from opium while the opioid definition would remain the same. Again, this is entirely speculation and well outside my field.

So I wrote that comment while reading the question in the review queue, which doesn't show the answers (like the answer which essentially says the same thing). I'll leave it since it doesn't hurt anything.

@canadianer thanks for your comments, and for the heads-up that there is a close vote. In many SE sites if it is not completely clear what one is asking, someone will first leave a comment asking for clarification, before reaching for the close button. I feel that silent, anonymous "unclear" voting is not productive behavior when the question is in fact fairly clear. One thing that demonstrates that is the lucid answer posted. I am not sure if it is 100% right yet, but it addresses all aspects of my question squarely.

@canadianer great minds...

First there was opium. Then the active components of opium (morphine etc.) were defined and called opiates. Then the receptors for opiates were discovered, along with their endogenous ligands (enkephalins etc.), and since those endogenous ligands were not derived from opium and indeed (being peptides) were not chemically related to opiates, a new term was needed. This term was opioid, and yes, the definition of an opioid is that it is something which binds to an opioid receptor.
The perceived circularity lies in the shift of emphasis from the drug to the receptor as the central player - when the first binding studies were being done in the early 1970s the search was for opiate receptors, not opioid receptors.

The only issue I have with this answer is that endorphins, enkephalins, etc. are not listed as opioids but as "opioid peptides" (most commonly), "opioid neuropeptides", or opiate-like pentapeptides or some such, as far back as 1977. So far, I have not seen them referred to as opioids.

@anongoodnurse Ref 2 of the WP page for opioids is as follows:  Hemmings et al.  (2013). Pharmacology and Physiology for Anesthesia: Foundations and Clinical Application: Expert Consult - Online and Print. Elsevier Health Sciences. p. 253. ISBN 1437716792. "Opiate is the older term classically used in pharmacology to mean a drug derived from opium. Opioid, a more modern term, is used to designate all substances, both natural and synthetic, that bind to opioid receptors (including antagonists)."  [my emphasis] ...

...I think the use of the term 'opioid peptide' is just a way of emphasising what is being discussed in a specific context.

Perhaps, but a Google Scholar search of 2016-2017 Neuropharmacology papers on opioids fails to refer to any endogenous opioid peptides as "opioids".

The introduction to this paper  – Involvement of Endogenous Enkephalins and β-Endorphin in Feeding and Diet-Induced Obesity – refers to opioid peptides as: endogenous opioids (twice); endogenous opioid peptides; endogenous ligands of opioid receptors; endogenous opioid activity; and finally states that 'This study aimed to distinguish the role of the two major classes of endogenous opioids acting at MORs and DORs, namely enkephalins and β-endorphin...'.


text:
How do leafcutter ants choose what plants to cut?
I know that leafcutter ants don't actually eat plants and only use them to harvest fungi. How do they choose what plants to cut?
They won't touch anything in my garden, but if I plant roses, they'll completely wipe all the leaves and petals in a single day.
If some plants are better suited than others for their "farming", how do they know them?


text:
Does any molecule other than DNA have a double-helical structure?
DNA is known to have a double-helical structure. Do any other molecules have this structure?

Probably also interesting to ask: was their molecular structure known before that of DNA?

Double Stranded RNA Actin Filament Collagen protein Starch is kind of similar too

A few examples:

Starch
A polymer of glucose that can form a double helix and functions primarily as energy storage in plants.

[image source]

f-Actin
Filamentous actin forms a helical structure with two strands of polymerized g-actin. This is a structural component of the cytoskeleton.

[image source]

Coiled Coil
Protein motif with a helical structure formed by two (or more) α-helices. Coiled coils are found in a diverse range of proteins from structural proteins like keratin to transcription factors like c-Fos.

[image source]

Gramicidin
A peptide-based antibiotic that has been shown to form membrane spanning double helices.

[image source]

Yes, double-stranded RNA as found in some viruses.

Do you know of any other such molecule? RNA is very similar to DNA, but is there a molecule that is very different from DNA and yet still has a double helix structure?

Yes, I thought you'd be only half satisfied with this answer. I do not know of any other molecules (but I am not a good chemist) but the answer may depend upon how different the structure of a molecule can be until you start considering its structure to really be different.

The structural protein collagen consists of a triple helix of polypeptides. Whether this answers the question is arguable—you could say that the triple helix contains double helices. In any case, depending on what prompted your question, I thought it might be an interesting structure to consider.


text:
Non-cavitating ultrasound for denaturation of short strands of DNA (~20 bp)?
I know that there is existing research on ultrasound-induced transient cavitation bubbles that mechanically denature DNA by generating violent shock waves locally in solution.
I would like to know if it is possible for non-cavitating ultrasound to denature short strands of DNA, ~20 base pairs in length (please cite sources, if possible). The mechanism should be mechanical, without involving thermal or cavitation effects of ultrasound. The ultrasound acts as a pressure wave, of the order of 10 MPa, and the DNA helices require a force of ~15 pN to initiate unzipping. I just need proof that this has been successfully demonstrated.
Thank you in advance.

Does DNA denature?


text:
Variations in asexual reproduction
It has always been said that sexual reproduction produces offsprings which are superior to their parents, due to the variations which they acquire causing them to survive better in their environment. That's because we can think of meiosis occurring at some level of their life cycle resulting in the variations in the final offspring.
 But what when we talk about bisexual organisms, might they be plants, animals or any other life form? Can't there be variations in their offsprings if they produce them asexually? It's like when they undergo gamete formation in different male and female structure present in that single parent, they'll surely undergo meiosis(if the parent is not haploid undoubtedly) forming the gametes which are dissimilar in their genetic makeup. When these fertilize, shouldn't they show variations?

The question is rooted in a misunderstanding of what sexual reproduction is and is not.
Any good intro book to evolution has a chapter on the diversity of reproductive systems. Consider for example Evolution: Making Sense of Life. If you speak french, the book évolution biologique has a very chapter on the diversity of reproductive systems. If you want something more complete and more advanced, you can have a look at The Evolution of Sex Determination.

It has always been said that sexual reproduction produces offsprings which are superior to their parents, due to the variations which they acquire causing them to survive better in their environment.

Who said that? The common simplistic idea and sex increases mean fitness because it increases genetic diversity is both wrong because sex does not necessarily increase genetic diversity and wrong because increase in genetic diversity does not necessarily result in increasing mean fitness.
You can have a look at the work of Nick Barton, Sally Otto and many others on the subject. The above misconception is well explained in the introduction of this talk from S. Otto's

[..] But what when we talk about bisexual organisms, might they be plants, animals or any other life form?

I'm not sure what you meant here. You probably did not want to use the term bisexual. Maybe you meant dioceous.
Please note that sexual reproduction does not mean dioecy. Sexual reproduction does not even mean anisogamy and doe snot necessarily involved more than one individual (see selfing).

Can't there be variations in their offsprings if they produce them asexually?

There is a whole range of reproduction mode and saying sexually vs asexually is making gross categories that make it sometimes hard to really answer the question. It is also hard to know what you mean by "variations" here. But shortly speaking:
Asexual reproduction does not necessarily mean total absence of recombination (see for example Narra and Ochman 2006) and definitely does not mean absence of mutations (see for example Sniegowski et al. 1997).

It's like when they undergo gamete formation in different male and female structure present in that single parent, they'll surely undergo meiosis(if the parent is not haploid undoubtedly) forming the gametes which are dissimilar in their genetic makeup. When these fertilize, shouldn't they show variations?

If there is fusion, then there is sexual reproduction, even if it is selfing and even is they don't have genders (anisogamy).

Thanks for the answer, it had literally cleared many of my misconceptions. I agree with your point that sexual reproduction doesn't always result in better offspring but can you please explain what you meant by 'sex does not necessarily increase genetic diversity'? I mean it does create variations. By variations I meant genetic recombination. I'm not sure what you meant here. You probably did not want to use the termbisexual. Maybe you meant dioceous. No I mean the use of term bisexual and an explanation to this was selfing as I well understood it.

Maybe you meant hermaphrodite by saying bisexual. Bisexual is a term mainly used for humans in sociology and does not mean being able to reproduce with oneself (selfing when there is fertilization) and does not mean having both sexes (hermaphroditism, usually called intersex in humans) either.

Recombination does not necessarily increase genetic variance in the population. It rather diminish it actually. It is a common misconception that sex necessarily increase genetic variation. Have a look at the link to Sally Otto's talk, that will probably clear things up.

The problem here is simply that you are considering self-fertilization as an example of assexual reproduction, when it's not the case.
Here is an oversimplified explanation, that may help you:
Sexual reproduction is a form of reproduction in which there is genetic recombination (unlike assexual reproduction).
Regarding the origin of the gametes, sexual reproduction can be classified as:

Cross fertilization: each gamete comes from a different individual.
Self-fertilization: both gametes come from the same individual.

Contrary to common belief, most hermaphrodite animals (what you call bisexual)  and most monoecious plants perform cross fertilization, not self-fertilization, but some of them do perform self-fertilization. However, self-fertilization is a type of sexual reproduction, not assexual.
Therefore, next time you read about a hermaphrodite (like the tapeworm Taenia, for instance) doing self-fertilization, remember: that is sexual reproduction, not asexual.


text:
How does the measeles virus form?
I would like to understand how (if possible) the measles virus could start to infect a population that was theoretically isolated from any other population group. Put another way, can the measles virus develop within a person without external influence/inputs?

Is the question "Can a measle virus be created anew and not via reproduction from another virus?" (the answer would be 'No').

So it is not possible for an isolated population to have instances of measles unless they are exposed to it from an external source, correct? I understand that it is an endemic disease, but my confusion is on how a population gets the first instance. Is there a better question I can post to get at that idea? I am interested in measles particularly.

You should have a look at an intro course to evolutionary biology such as understanding evolution by UC Berkeley for example. There is no clear first instance. Modern day measle viruses evolved from an ancestor that was not the modern day measles. In any case, there is no spontaneous generation.

@Remi.b, okay, if you want to post this comment as an answer then I can accept it as the answer and close this out. Thanks.

While the question is clearly quite introductory, I think it can be answered in the broad sense and should not be closed as off-topic. I also think that two down votes is a bit harsh.

The question could be rephrased
Can a measle virus be created anew and not via reproduction from another virus?
The answer to which is "no".
The falsified idea that new life forms can jump pop up out of nowhere is called spontaneous generation. Spontaneous generation do not occur.
Note however that sometimes it may look like as if a new epidemic came from nowhere. The reasons is due to natural reservoir.

A natural reservoir  or nidus (the latter from the Latin word for "nest") is the long-term host of a pathogen of an infectious disease.

An asymptotic carrier can be used as a natural reservoir

An asymptomatic carrier (healthy carrier or just carrier) is a person or other organism that has contracted an infectious disease, but who displays no symptoms.

These reservoirs can keep the viruses (or other pathogens) alive in while from the outside it looks like the disease has been eradicated. At some point the virus can spread again making it feel like it came out of nowhere.
[..] my confusion is on how a population gets the first instance
There is no clear first instance. Modern day measle viruses evolved from an ancestor that was not the modern day measles. Just like there was no sudden first human (or any other species). There were just ancestors that evolved to become what we now call modern day humans.
You might want to have a look at an intro course to evolutionary biology such as understanding evolution by UC Berkeley for example.

I'm somewhat regretful of my final close vote and I nominated for reopening based on your comment above. I think you could add to this answer a brief note on reservoir species and asymptomatic carriers, and how either can sometimes contribute to apparent outbreaks of disease from "nothing", though neither is thought to contribute in the specific case of measles.

@BryanKrause Thanks a lot for the helpful comment.


text:
Effect of UV radiation on retinoid (vitamin A) receptors in the skin
The retinoid receptors in the skin (face) can be disabled by UVA sun radiation as these study states : https://www.sciencedaily.com/releases/1999/03/990331063314.htm
In this article it says the same : http://www.abc.net.au/news/science/2015-11-18/how-uv-light-damages-our-skin/6856742

" UVA activates receptors that produce the enemy of firm skin: matrix metalloproteinases. These enzymes have one job and they do it beautifully: breaking down collagen. And it doesn’t take much UV at all to get this going, so even without sunburn any parts of your skin that are exposed to the sun will age.

As if the collagen attack wasn't insult enough, UV radiation also interferes with the production of Vitamin A receptors on our skin cells.
Vitamin A is critical for cell growth in our skin, but without functioning receptors for the vitamin to activate, our skin ends up thinning, and that’s something no amount of carrots can fix.
Question is: do these receptors actually work again after sun exposure is stopped? Or any topical/oral treatment with vitamin a will be useless for skin regeneration?
Thank you

Please do not write titles like this again. It appears as a shameless attempt to draw attention to your question. I have given it a minimal edit rather than voting for it to be removed. Please take note.

@David The title stood to be improved, but the original doesn't appear to be at all untoward like you've indicated... certainly not "a shameless attempt to draw attention". Maybe just silently improve it next time instead of admonishing a new user unnecessarily.


text:
Why does alum work on blisters in the mouth/cold sores?
Alum used to be an age old tradition to treat sores in the mouth and it worked beautifully.Foes anyone know why Alum works on sores in the mouth ?

Welcome to SE Biology. Please take the guided tour and then read about how to ask a good question. You will see that you are expected to "Search and Research" before posting. Have you done this? If the articles you have found don't answer your question, reference them, say what they do say and why that is insufficient. Otherwise I am afraid your question is likely to be removed.

Alum has been shown to be effective in treating aphthous stomatitis (canker sores) and it is believed to be due to the compound's significant drying effect. Alum is known as an astringent - a chemical compound that tends to shrink or constrict body tissues. More information on alum's astringent properties are reported in this paper. As the infected tissue shrinks there is a decrease in pressure due to swelling and this less pressure around the nerves in the affected area. The exact mechanism is still under question.


text:
Cell biology - Resting membrane potentials
Why do we say there is an overall negative charge on the intracellular side of the plasma membrane at rest, and an overall positive charge on the extracellular side when both potassium and sodium are positively charged ions, and they are in relatively equal amounts on either side? It seems to me that both sides should be positively charged, and I can't get my head around it.

great question... with an equally great answer... where have you looked for this answer?

The resting membrane potential is the voltage at which there is no net flow of ions across the membrane.
Every ion will tend to flow down it's concentration gradient (this is just a basic principle of physics/chemistry). So, without considering charge, for a typical cell, potassium will tend to flow out, sodium will tend to flow in, and other ions will also behave according to their concentration gradients.
The other crucial part of the equation is the relative permeability of the membrane to each ion. This comes mainly from the presence of ion channels. At rest, a typical cell has more permeability to potassium than sodium.
That means that if the driving force for sodium and potassium is the same (it's not identical at 0 mV but fairly close), more potassium will move than sodium.
If the definition of resting potential is the potential where net flow of charge is zero, and considering only sodium and potassium, then rest has to be where sodium flowing in equals potassium flowing out. This situation occurs when the inside of the cell is negatively charged compared to the outside: the membrane voltage "holds" potassium in and "pulls" some sodium in, such that their currents are equal and opposite despite the higher permeability to potassium.
Note that the voltages we are talking about in neurons, on the order of 10s of mV, are very small, and electrical forces are very strong. The concentrations of positive and negative ions are almost exactly identical on both sides of the membrane: only a few ions actually have to move to make a (biologically) large membrane voltage. What is actually important is the permeabilities: that's what makes action potentials and other forms of neuronal signaling feasible.

I had the same question and wanted to re state the answer with more steps. This might be helpful as I had no idea what was going on and this will explain some common misunderstandings that I and probably most people have with this.
At resting potential we have Na+ in the exterior and K+ and organic acids in the ctyosol. The membrane potential relies on electrochemistry to propagate a signal from dendrite to distal synpase. To propagate neuron signals it would not be ideal to transport these anions across the membrane given their size and utility inside the cell. It would be slow and require intensive transporters in the membrane. We can however use cations which are relatively abundant, small and with relatively low thermodynamic cost.
The -70mV resting potential describes the relative charge state across the membrane. It describes that the cytoplasm is relatively more negative compared to the extracellular fluid. Since we have organic acids giving the cytosol a slight negative character, we can use the thermodynamics of diffusion to our advantage. This is where our cations come in to use. At rest we balance the concentrations of cation movement across the membrane via the sodium potassium ATPase which maintains the gradients of Na (high on extracellular side) and K (high on cytosol side). We only need the balance the movement of these cations to create the polarised character on either side of the membrane given the organic acids.
When a dendrite receives excitation signals Na+ transporter proteins open and sodium rapidly enters the cytosol across the gradient. The potential falls as the cytosol becomes more positive and we have a change in the potential (action potential).
This doesn't explain why K+ is needed here. Propagation of the signal along the neuron requires the cytosol beside the site of action potential to change potential and become more positive. Diffusion takes time. If we reverse the Na pumps and immediately removed all Na+ from the cytosol this wouldn't create the necessary change in potential along the neuron because the Na+ is being pulled into the extracellular space rather than given the time to move along the cytosol.
K+ plays the role of repolarising instead. While Na+ allows the signal to propagate, K+ is moved out of the cytosol into the extracellular space to move the potential back to -70mV. When the signal is sufficiently distal, Na+ can then be moved to the extracellular space and the resting potential can be restored.

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


text:
Are these birds in video real? What are they called?
I recently came acroos this video   :  https://m.facebook.com/story.php?story_fbid=1053324651468913&id=492140647587319
I want to know whether these birds are real or edited? If they're real,  what are their names?

The problem here is that your question depends on a video on another site and so is not a self-contained question here. Unless you can at least present some screen captures to illustrate the problem, it is likely to be closed.

Have been to many stackexchange sites,  have seen many such questions (& answers,  too), so I thought it was okay...  Moreover, taking ss would probably be illegal....!

I don't care who else breaks the rules. I am only concerned with applying them, and educating others to apply them, to questions I encounter as a reviewer on this site. There are many more violations than there are reviewers to deal with them. If you can't post a question in a way you consider legal don't post it at all. I vote to close this question as unclear.

@David Actually, I would like to keep this question open.  It could have been better, but I think the answerer gave us sufficient context  so it will continue to be useful for people.

@tbek — OK. I'll reverse my vote.

Somehow I found my way back to this question and would like to apologize for not asking the question in best possible way. However I'd like to note that I didn't even know, at that time, that I can find those birds over their (or the fact that such beautiful creatures do exist, and hence my question) and my question was motivated by the opportunity to search about them if at all they were real. I'd like to thank the user24284 for showing me "where to search" also.

Yes, they are real, that's not a CGI. That footage belongs to The Cornell Lab of Ornithology, and those are birds-of-paradise.
The first one is a Wilson's Bird of Paradise (Diphyllodes respublica). Here is an image of it:

The second one, showing a courtship display, is a Superb Bird of Paradise (Lophorina superba). Here is an image of it:

And the courtship display:

The third one is a King Bird of Paradise (Cicinnurus regius). Here is an image of it:

The next one is the Wahnes's parotia (Parotia wahnesi). Here is a picture of it:

The last one is a King of Saxony Bird of Paradise (Pteridophora alberti). Here is its picture:

Finally, here is the only correct way (just kidding) to watch any video with birds of paradise: narrated by David Attenborough! Have a look:
https://www.youtube.com/watch?v=nWfyw51DQfU

At this point, I wanna tell you, you just left a couple or so birds more...really waiting to know more about all of 'em! And +1 of course ;)


text:
Electric Shock To Human Body
What happens in our body when we get an electric shock?

Many different things happen, and there are various reasons why people survive.

Ok. So, first of all, it depends on the power of the shock.
This relates to volts (electrical pressure) and amps (amount of electricity)
I strongly suggest you read
this article
That article explains what happens in great detail, but if you're still curious, here are some other things that would obviously happen:
If it is a constant DC Current, negative ions will rush to the anode, and positive ones will rush to the cathode. The negative ions (including oxygen and chlorine) will bleach the cells in the area and kill them.
The positive ones in the cathode area will raise the ph drastically and liquefy the adjacent cells.
If the current is high enough, the cells will heat, which will denature the proteins and enzymes within and kill them.


text:
Mitosis in free nuclear divisions
When free nuclear divisions occur(for instance in endosperm formation in coconut etc)....there are many nuclei undergoing kartokinesis at a given point of time...so that means each karyokinesis will naturally have to involve spindle fibre formation for the chromosomes to be pulled apart in anaphase....so when there are no cell walls or barriers and so many sets of spindle fibres...how is it that the spindle fibre of say dividing nucleus 1 doesn't go and attack to the chromosome of another dividing nucleus....shouldn't there be utter chaos out there as every spindle fibre can attach to any chromosome of any diving nucleus.....I hope you have u der stood my question

No one knows about this?


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Help ID this plant with balloon-like feature containing seeds
I noticed this plant creeping over another Ipomoea quamoclit near my house in Kerala, South India. It has these balloon-like projections over them that break when popped. These projections do bear seeds. No visible flowers.
Leaves:

The balloons:

The seeds:

EDIT: This plant is a creeper, obviously.

I searched Google for Lantern plant and came across this http://tabibito.hopto.org/display_one_file.php?article=494

Which is the same plant, but not the best of references, it doesn't give a scientific name and I am not sure Paper lantern plant is their right identification.
It is definitely of the genus Physalis
https://en.wikipedia.org/wiki/Physalis
but as yet haven't been able to find the species that matches your leaf exactly. But I'd thought I'd post for now as it may help you, or others.

Thanks! I suspect it belongs to the Physalis genus too.

I don't think the leaves match,this not the exact species but sure it belongs to physalis


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The advantages of using a strand specific cDNA in RNA-Seq?
May I ask what are the advantages of using a strand specific cDNA library in an RNA-seq experiment? as far as I know it can make us able to read the code region but what about other advantages?

Welcome to SE Biology. Please take the guided tour and then read about how to ask a good question. You will see that you are expected to "Search and Research" before posting. I quickly found a paper on this topic by Googling. If the papers you have found don't answer your question, reference them, say what they do say and why that is insufficient or not what you are after. Otherwise I am afraid your question is likely to be removed.

Hi, I have already google it before posting this question but it is still not clear to me what are the other advantages. Even when you think my question could be basic and silly I still need someone to answer this question in a simple way please.

It is not a question of whether the question is basic or silly, and I did not say that. What I did was review your first post — as is standard practice here — and explained how the site worked giving links, using standard language. I know you haven't completed the introductory tour as you do not have the badge for doing so. If you want to use this site you must follow its rules. Please read them.


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Why do cherries sometimes grow as triplets?
Usually when I think of cherries, I think of them as pairs. I think most of us imagine them that way, but recently, I stumbled on a picture of a triple cherry:

Which I found interesting, but I couldn't find any more info on this, so I hoped to find some answers here. Why do they sometimes grow like that and how often does it happen compared to their regular twin counterparts?

Why do they (cherries from a cherry tree) sometimes grow like that (in triplets) and how often does it happen compared to their regular twin counterparts?

After doing a considerable amount of research, I also wasn't able to find much of any literature that addresses your question, aside from this. From that article it says:

When you think of cherries you imagine them in pairs, don't you? It's also common to find cherries grouped in quadruplets on a single bunch of stems. This happens because of the way cherry flowers bloom -- several pink blossoms grow from a single focal point, and when those flowers wilt and become fruit, the resultant cherries are connected, too. It's smart to keep cherries attached to their stems whenever possible, as they will stay fresh for much longer. And when you're harvesting the fruits, harvest the cherries at the stem (no higher!) or you risk next year's buds snapping off along with them.

The bolded section seemed to be most revealing, and so, I was able to find a time-lapse video that depicts the various stages of the flowering & fruiting process for a cherry tree. The video is only 4 minutes long, and I highly suggest watching it.
From watching the video, it can be confirmed that the statements made by the previously quoted passage are true -- "several (pink) blossoms grow from a single focal point, and when those flowers wilt and become fruit, the resultant cherries are connected, too".
Consider the following series of images, which are screenshots from the time-lapse video. You should view these images in an alternating left to right, right to left fashion, going from top to bottom (so, snake-shaped).

As can be seen, each flower does grow from a shared focal point, and, the cherry fruit does originate out of the exact same location as where the flower was.

What's most interesting to note, and which begins to answer your question, is:
When viewing the third row (left to right), for the first two images, there are multiple cases of three cherries growing from the same stem. However, in each case, one of the three cherries are actually extremely underdeveloped. But then, if you compare the second and third image (still in the 3nd row, left to right), those underdeveloped cherries completely disappear!
It would then seem to me that, since one of the three cherries are severely underdeveloped (most likely due to limited nutrition & resources), the farmer who is tending to the tree will prune these (underdeveloped) cherries, thus leaving only pairs of two. In extreme cases, perhaps, the third (or even fourth) cherry achieves enough development for the farmer to not consider pruning it, but, this appears to be the exception.
Further supporting this idea, consider the next series of screenshots (from the same video).

When harvesting, the farmer deliberitely picks the cherries by pairs of two. There's even a time when he almost pulls off three, but then makes sure to leave the third. This process of pruning underdeveloped cherries, as well as harvesting in pairs or two, is most likely common practice amongst cherry growers.

And when you're harvesting the fruits, harvest the cherries at the stem (no higher!) or you risk next year's buds snapping off along with them.

Given that quote, it could be that picking in pairs of two is the most efficient method of harvesting that also best ensures the safety of next year's buds. So, to restate the reason, it would appear that cherries are rarely seen in groups of three (or more) due to nutritional constraints, and the pruning & harvesting methods of the farmer, or tree owner.

I doubt anyone can top that answer, so I'll just accept it. Glad to see I wasn't the only one struggling with finding anything regarding this topic. Thanks for your detailed answer!

The answer is close, but actually, it isn't the farmer that prunes the underdeveloped cherries. Cherry trees drop underdeveloped fruit on their own as a way to thin production down to what the tree can support. The more cherries on the tree, the smaller they will all be. So trees drop smaller fruit and excess fruit for the benefit of the remaining crop.


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Can memories intentionally be overwritten, or forgotten?
Over the years, I've come across studies (e.g., here, here, and here), and have watched documentaries (similar to this), that speak about memory retrieval, and how that, every time you recall a memory, that memory is subject to being distorted (less accurate). Of the different types of memory, it seems that this is most often spoken about when episodic memory is involved.
In pretty much every situation I've seen, the person with the memory is trying their best to most accurately recall that memory, with respect to the true event(s) that was originally experienced. However, would it be possible to intentionally cause memory distortion, perhaps by continuously recalling a memory and then deliberately thinking of false information? Or, can this process only happen subconsciously?
There is a movie that somewhat plays on this idea, Eternal Sunshine of the Spotless Mind. In this movie, a participant is alseep while wearing a kind of helmet that selectively targets and erases desired-to-be-forgotten memories. And though my initial curiosity did not arise from seeing this movie, and yes, I am aware that this movie is sci-fi, I do still wonder if this kind of overall effect could be achieved without technological/medical intervention. If not, why?

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


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Stability of the chromosomes of thermophilic bacteria
We know thermophiles — generally archaebacteria — can survive high temperature, but their genomic DNA also contains hydrogen-bonded nitrogen bases. Why don't they collapse like ordinary hydrogen bonds?

The stability and replication of the DNA of thermophiles is an interesting problem, for which there does not appear to be a single unequivocal answer. However the way you express this question is unfortunate: the hydrogen bonds in the DNA of thermophiles (which include some eubacteria as well as archea) are the same as those in any other genomic DNA. The question is, rather, why the strands of the DNA do not dissociate. This is not really my area, but as there have been no other answers I shall summarize what I have learned from the literature.
A review that was the starting point for this information is:
D.W. Grogan, Hyperthermophiles and the problem of DNA instability Molecular Microbiology (1998) 28(6), 1043–1049.

One obvious possibility would be that the genomes of thermophiles have a high percentage of GC, as GC base-pairs have three hydrogen bonds, whereas AT base-pairs have only two. However, this is NOT the general case.
It has long been known that the melting temperature (the temperature at which 50% strand-separation has occurred) is increased by increased concentration of cations. It has been suggested that this could be a factor, especially in those thermophiles that are also extreme halophiles.
In eukaryotes genomic DNA is condensed into chromatin by the interaction of the basic histone proteins. These proteins are not found in prokaryotes, but different basic molecules, polyamines, have been observed that are more abundant in thermophilic than mesophilic bacteria. As they have been observed to protect DNA from thermal denaturation in vitro, it has been proposed that they may also perform this function in vivo.
Type I topoisomerases that introduce positive supercoils into DNA (‘reverse gyrases’), occur in hyperthermophiles examined but not in mesophiles, and it was suggested that this could stabilize the DNA. However, the Grogan review presents a body of evidence that casts doubt on whether this is, in fact the case.
In addition to strand-separation, the genomes of thermophiles face the problem of increased damage to their DNA. Although, again, the situation is complex, it appears that they have evolved more extensive and active systems of DNA repair to deal with this.


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The genotype of a hybrid plant from a cross and its determination?
Question
I know about crosses Inheritance and this question is about Test Cross.
I want to know if we can determine the genotype of hybrid plant by crossing with a pure recessive parent from Filial generation 1 or if we require more generations to know the genotype?
My thoughts
if the plant is homozygous then no need if it is dwarf as we know that dwarf genes are recessive but if the phenotype is tall then we have to find its genotype whether it is Tt or TT. I have come across a MCQ : the genotype of hybrid plant obtained from a cross can be determined by crossing the plant with - . To me the ans should be Pure recessive parent at F1 generation. But ans given is Pure recessive parent at F2 generation

If you both parents are homozygous (which is the consequence of being a pure line), then you don't need to even do any cross to infer the genotype of the F1. Maybe you should give an example as to clarify your question and try to solve it yourself so that we see where is your misunderstanding

@Remi.b Yes, if the plant is homozygous then no need if it is dwarf as we know that dwarf genes are recessive but if the phenotype is tall then we have to find its genotype whether it is Tt or TT.   I have come across a MCQ : the genotype of hybrid plant obtained from a  cross can be determined by crossing the plant with - .  To me the ans should be Pure recessive parent at F1 generation. But ans given is Pure recessive parent at F2 generation.

I added your comment into your post and created two sections. Feel free to roll back if you don't like my edit.

@Remi.b Thank you for the edit, now the post looks more appropriate. Now, If we look at the question from statistical view the ans looks simple that more data sampling means more reliable effects i.e F3, F4.... generations, as the same done by Mendel. So, as we know in MCQ there is one correct ans either we gain or loose mark. Little caution, if you have to choose from two above options, which you will choose?

Real genetics is complicated
Biology is more complicated that you seem to expect. The answer very much depends upon the underlying genetics of the trait (and the underlying non-genetic factor affecting the trait; see here) as well as the genotype you are crossing it with.
Simplified model
But let's assume an extremely simple model of pure dominance / recessivity at a single bi-allelic locus. Let a be the recessive allele and A be the dominant allele. Let's assume the pure line you are using for the crossing is homozygote for the a allele (and let assume that we know it).

If the parent is AA, then all offspring will be Aa and all will have the dominant phenotype.
If the parent is Aa, then 50% of the offspring will be Aa and have the dominant phenotype and 50% of offspring will be aa and have the recessive phenotype.
If the parent is aa, then all offspring will be aa and have the recessive phenotype.

So, under this simple model, if you can produce a high enough number of offsprings to make good statistics, then yes, looking at the F1 generation is enough to determine the genotype of the parent.
Under a more complex model, it is not necessarily possible to only look at the F1 generation.

The concept of a test cross is still relevant. It was on my US medical licensing exam. Though that was quite a few years ago, I hope it is still on it. It is still important for evaluating risk based on family history. There are a number of diseases that demonstrate Mendelian inheritance. You can't just run genetic tests on everyone.

I'd add that a test cross is very specific: it's a parent that doesn't show a recessive trait crossed with a parent that does (just the first two bullets in your answer).


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ID for red millipede swarm near my place
Location:Hyderabad,South India.
These worms usually come out when it rains,these worms are the most common ones any help in figuring out them,they come in groups too.

Certainly a swarm of some Diplopoda species. Couldn't identify them any better, though. Video, other photos, news report.

Based on the body structure and double pair of legs per body segment, this is a millipede.
Based on the small size and spacing between body segments, it could possibly be in the Paradoxosomatidae family. You could check by examining the specimen more closely:

Most species possess a groove or furrow ("sulcus") on the dorsal surface between the keels (paranota) on each segment.

National Geographic ran a story/video on swarming Paradoxosomatidae in Senegal in 2017:

Some species swarm together during mating season or to hunt for food, and some studies have theorized juveniles swarm together for protection from predators.

Bellairs et al. (1983)1 studied a similar swarming species of millipede in India:

The adults of Streptogonopus phipsoni (Pocock), an Indian polydesmoid millipede, emerge from the soil at the onset of the monsoon and mate. Eggs are laid in the soil and the adults die. The larvae leave the soil at stadium III and, apart from moulting periods, remain on the surface until the end of the monsoon. The larvae are aggregated in swarms, usually consisting of several hundred individuals. They are active on open ground, including metalled roads, during daylight, but usually spend the night in an inactive state under cover of stones or vegetation. If a swarm is disturbed, the individuals scatter but later reaggregate.

 Source: Bellairs et al. (1983)
I couldn't find any additional reputable (or really much of any) detail about S. phipsoni in English sources online. So I think I'll leave you with this information for you to explore in your native language more closely.

Though, Bellairs et al. cite Hoffman (1980) 2 and Attens (1937) 3 as their identification sources.
Also, Golovatch & Wesener (2016)4 provide a relatively up-to-date species checklist of the millipedes of India, so I'm certain that reference would be a good place to continue learning more.

 Citations:
1  Bellairs, V., Bellairs, R. and Goel, S., 1983. Studies on an Indian polydesmoid millipede Streptogonopus phipsoni Life cycle and swarming behaviour of the larvae. Journal of Zoology, 199(1):31-50.
2  Hoffman, R. L. (1980). Classification of the Diplopoda. Geneve:  Musee d’Histoire  Naturelle
3  Attems, C. (1937). Myriapoda 3. Polydesmoidea 1 Fam. Strongylosomidae. Tierreich 12:1-300.
4  Golovatch, S.I. and Wesener, T., 2016. A species checklist of the millipedes (Myriapoda, Diplopoda) of India. Zootaxa, 4129(1):1-75.

@SonicSplasher please consider accepting ("checking") my answer if it adequately answers your question. If it does not, please let me know what lingering question/doubt you have and I'll try to address it if appropriate or possible.

I am really sorry for responding this late, I had life stuff to do and totally forgot about stack.exchange. I'll review this and let you know fast

As soon as I spot these badboys, I'll take a few and probably try to identify them from a checklist of characters.

Streptogonopus phipsoni, probably IV or V stadium.
For reference, see: Bhakat, S. (1987) and other

for a reference, it is very helpful to include a web link. Lacking a web link, a full reference (e.g. journal, publisher, title) would help the asker to evaluate this answer.

you are bhakat.s


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Plant growing very rapidly near my house
please see attached photos of a plant, that is growing rapidly near my house. All my friends failed to classify this plant. Can any botanist/biologist help to discover the species of this plant?
Thank you in advance!

Help us. Where do you live?

It looks like a young Empress Tree (Paulownia tomentosa)
Native to China, it is an invasive species in the USA. looks beautiful when full grown however


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Which mushroom could be this?

Collected in northern West Europe in autumn 2017

It's a shelf mushroom (pores or tubes on the underside) or polyspore (are also called bracket fungi.) How specific an answer do you want? Some are edible (e.g. 'chicken of the woods'), some are lethal.

By a hint from a FB forum, it should be meripilus giganteus and I have to agree.


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Have there been any study that document the evidence of the changing ratio of the biomass of different trophic levels?
You would expect a number such as the producers (photosynthetic) biomass to consumers + decomposers biomass ratio is a very important indicator for sustainability. It is also very probable that the ratio has been changed due to human activities (land clearance, animal agriculture etc.) which have resulted in the likes of climate change (which is in a sense just a problem of excessive mineralization (both industrial and biological) relative to immobilization by producers). Have there been any studies that try to calculate and monitor this number? I can't seem to find any.

Related: In a typical model ecosystem, what might the percentage of plants be to top predators and everything inbetween?

Related answer to References concerning the relative population sizes of predator and prey, specifically dealing with biomass scaling of predators and prey.


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How different are these terms: Phylloclade, Phyllode, Cladophyll and Cladode?
We started with Plant Morphology in class (specifically, the morphology of angiosperms).
My teacher's provided us with the following terms and their definitions.

Phylloclade
A modified stem that is flattened or cylindrical and capable of unlimited growth. They are green and capable of photosynthesis. Examples include; Opuntia, Epiphyllum, Casuarina, Euphorbia.
Cladophyll (also called a Cladode)
A modified stem capable of limited growth. They are green and capable of photosynthesis. They bear an axillary bud at the their middle, from which flowers develop. Examples include; Ruscus, and some Asparagus species.

 No mention of the term "Phyllode"...yet.

Now I'm sure I understand the definitions provided, however, I'm beginning to seriously question the validity of those definitions.
Apparently, these terms aren't documented very well, and after two hours of constant Googling, I arrived at:

Phylloclade (From the Wikipedia page of the same name)
Phylloclades and cladodes are flattened, photosynthetic shoots, which are usually considered to be modified branches. The two terms are used either differently or interchangeably by different authors. [Examples provided]: Ruscus, Phyllanthus and some Asparagus species.
Cladophyll (From the Wikipedia page for "Petiole")
In some plants, the petioles are flattened and widened, to become phyllodes or phyllodia, or cladophylls and the true leaves may be reduced or absent. Thus, the phyllode comes to serve the functions of the leaf. [Examples provided]: Some Acacia species.

This is annoying, seriously.
According to the definitions provided by my teacher, we're dealing with something called a "Phylloclade" and something else called a "Cladophyll" (= "Cladode"). They don't mention the term "Phyllode", though.
Based on the Wikipedia definitions, however, we're dealing with something called a "Phylloclade (= "Cladode", if you ignore minor d̶i̶s̶r̶e̶p̶a̶n̶c̶i̶e̶s̶  differences in their definitions, which are mentioned later on in the Wikipedia article), and something else called a "Cladophyll" (= "Phyllode")

My questions:
1) What are the correct definitions of the terms "Phylloclade", "Phyllode", "Cladophyll" and "Cladode"?
2) Are the examples (provided in my notes and the Wikipedia articles) actually relevant/correct? For example: Does Ruscus possess  Phylloclades (as suggested by the Wikipedia article) or does it possess Cladophylls (as suggested by my teacher)?
3) Building on question (1): Does "Phylloclade" = "Cladode", and "Cladophyll" = "Phyllode"?

there seems to be a discrepancy in the term cladophyll in thiswebsite it is a modified leaf but in thiswebsite it is a modified stem.

But my high school level textbook however claims cladophyll and cladode to be synonymous so it's a stem.. but the wiki page definitely says it's a leaf modification. This is ambiguous!

Apart from the discrepancy of the cladophyll term I can say that both your teacher and the wiki page are correct.
If you read the Wiki page carefully it states that

Phylloclades and cladodes are flattened, photosynthetic shoots, which are usually considered to be modified branches. The two terms are used either differently or interchangeably by different authors.

(As you have also quoted)
This is simple because both phylloclades and cladodes are stem modification for photosynthesis and xerophytic adaptation as well. So in this context they are interchangeable
Also if you have further read the article it states why the terms are interchangeable and why not. The different levels of definition are given:

Definitions of the terms "phylloclade" and "cladode" vary. All agree that they are flattened structures that are photosynthetic and resemble leaf-like branches.

one definition, phylloclades are a subset of cladodes, namely those that greatly resemble or perform the function of leaves,[2] as in Butcher's broom (Ruscus aculeatus) as well as Phyllanthus and some Asparagus species.

The definition given by your teacher can be interpreted by these two definitions stated in the Wiki page:

By an alternative definition, cladodes are distinguished by their limited growth and that they involve only one or two internodes.[3] By this definition, some of the most leaf-like structures are cladodes, rather than phylloclades. By that definition, Phyllanthus has phylloclades, but Ruscus and Asparagus have cladodes.

Another definition uses "phylloclade" to refer a portion of a leaf-like stem or branch with multiple nodes and internodes, and "cladode" for a single internode of a phylloclade.

But phyllode is a leaf modification, specifically a modification of the petiole for photosynthesis and a xerophytic adaptation to some extent. (Source is the Wiki page itself)
So to conclude

phyllode is completely different from phylloclade and cladodes.
Taking the type of morphology of the plant into consideration and the definition used, phylloclade and cladodes may be used interchangeably or may not be.

I will write an update if I find an answer to the discrepancy part

Just Remember the two main ; Phylloclade is a STEM modification for desert like area in which the stem becomes broad and fattened (in opuntia) or cylindrical(in euphorbia) !!
Phyllode is a LEAF modification and found in Australian Acasia in which the PETIOLE becomes a little braod and start performing photosynthesis!!
More key differences can be found on here https://www.differencebtw.com/difference-between-phyllode-and-phylloclade/


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Oxygen mask to patients
Why are oxygen masks given to patients? Can't they take in the  atmospheric oxygen? Also, why do they die if the oxygen mask stops providing oxygen?

these patients are being given oxygen in higher concentrations than the atmosphere contains. usually due to an in ability to uptake oxygen effectively.

Oxygen masks can provide up to near 100% oxygen, whereas the atmosphere contains only ~20%. Typically, oxygen is provided in cases where patients' blood oxygen saturation is low or is likely to be low.
Giving a patient supplemental oxygen helps them to achieve oxygen saturation even if their breathing or circulation is impaired, and allows slightly more oxygen to be dissolved in the blood, which can be helpful in cases of blood loss or other traumatic insults.
I'm not sure of any cases where patients simply die immediately if their oxygen mask fails, outside of movies/TV; it's more of an issue of trying to provide the best outcome possible in a difficult situation.
There are also some negative side effects of oxygen supplementation. Overall, Wikipedia has a reasonable overview of these, as well as the indications for oxygen supplementation.

70 children died in India because the oxygen supply was cut. Why did that happen?

I might have misread an immediacy in your statement (like they die immediately when oxygen is removed), based on the common media trope, not realizing you were motivated by a recent news event. The children most likely died because they had illnesses that prevented them from getting enough oxygen through normal breathing; supplemental oxygen could improve their blood oxygenation enough to keep them alive.  When the supplemental oxygen was withdrawn, they would asphyxiate.