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Understanding Enzyme saturation curve

From the above picture it can be seen that, in the region "B" the activity of enzyme is not proportional to the substrate concentration.
Why don't we achieve enzyme saturation linearly? Why do we go through that curved phase( region B )?
Why don't all enzyme gets saturated at a point?

The binding of substrate S to enzyme E is an equilibrium which means that there will always be some free enzyme (V is proportional to ES). Section A of the line isn't really linear at all.

At very high substrate concentration, the process will become diffusion limited. At that point adding additional substrate will no longer improve enzyme effectiveness, thus we get a curve and not a straight line as the enzyme concentration is constant.

Your image is not correct.
According to Lehninger (2000):

At relatively low concentrations of substrate, V0 increases almost linearly with an increase in [S]. At higher substrate concentrations, V0 increases by smaller and smaller amounts in response to increases in [S]. Finally, a point is reached beyond which increases in V0 are vanishingly small as [S] increases. This plateau-like V0 region is close to the maximum velocity, Vmax. (emphasis mine)

This is the image that comes after that paragraph:

FIGURE 6–11 Effect of substrate concentration on the initial velocity of an enzyme-catalyzed reaction. Vmax is extrapolated from the plot, because V0 approaches but never quite reaches Vmax. The substrate concentration at which V0 is half maximal is Km, the Michaelis constant.
Thus, regarding your questions ("Why don't we achieve enzyme saturation linearly? Why do we go through that curved phase( region B )?"), the answer is: there is no line, it's all curved.
Source:

Lehninger, A., Nelson, D. and Cox, M. (2000). Principles of biochemistry. New York: Worth Publishers.

But is this really an answer to the question? Despite his mistaken diagram, the basic point he is asking is why the curve is hyperbolic rather than linear. This, of course is trivial and answered in all texts, but an unhelpful answer really isn't a lot of use. Surely better to scrub the question.

OP accepted the answer. So, I guess the answer is fine.

@David I got my answer from another question's answer ( Mattdo's answer to https://biology.stackexchange.com/questions/9024/why-are-enzyme-catalysed-reactions-slower-at-lower-substrate-concentration?rq=1) Which put emphasis on diffusion. But I accepted Gerardo answer because it highlighted mistake and there was no other answer.

@JM97 Please unmark my answer as the accepted one, specially if you think that it was unhelpful. Normally, nobody writes another answer if there is already an accepted one. So, by unmarking my answer, you get more chances of receiving the answer you wish, whatever it is.


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Genomic control explanation
I am following the original genomic control article -
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.167.8448&rep=rep1&type=pdf
What's the role of $p_i$ in the article? It says that $p_i$ denotes the frequency of $A_i$ allele in population. Is it derived from Hardy-Weinberg equilibrium?
I would like to know how I should calculate $p_1$ for a specific data set.

I have not read the article but in general the allele frequency is pretty much the easiest statistics to compute from population genetics data.
The allele frequency $p_i$ of the allele $A_i$ is the relative frequency of this allele $A_i$ in the population. In other words, it is the counts of haplotypes having the allele $A_i$ divided by the total number of haplotypes. For the specific case of diploid organisms, this frequency is the count of allele $A_i$ divided by twice the number of individuals.
Consider for example the following data, where we have two alleles in the population, $A$ and $B$. Each individual is denoted by its two haplotypes separated by '|'. For example individual A|B is heterozygous.
A|B A|A A|A A|A B|B A|B A|B A|A A|A A|A A|A A|B A|A A|B
In this population there are $7$ Bs over 14 individuals. That makes a allele frequency for B of $\frac{7}{28} = \frac{1}{4}$.
Of course, if you have genotype frequencies, you could - making a number of assumptions - calculate the allele frequency using Hardy-Weinberg but typically from empirical data, you don't need to go through that.
More information about Hardy-Weinberg rule at the post Solving Hardy Weinberg problems.

source: Stack Exchange

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

sort: votes


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Large plasmid ligation: do I need alkaline phosphatase?
I have a doubt about a protocol I'm using for a ligation of a very large plasmid (15kbp circa) with an insert: after digestion with a single-cut enzyme (sticky ends), the protocol passes directly to the purification of the plasmid without making any alkaline phosphatase. My doubt is during the ligation, the plasmid will self-ligated without accepting the insert?. Am I mistaken or the protocol is incorrect?

A plasmid vector will always be prone to recircularisation when a single restriction enzyme has been used, but recombinant plasmids will also be formed during the ligation. Alkaline phosphatase treatment can be used as you describe; you can also  simply make sure that the insert fragment is present in high molar excess and be prepared to work harder at the end to find the recombinant plasmids. Neither approach is correct or incorrect, they both have their limitations.
Of course the best approach is to avoid this type of cloning altogether.
Added later
Incidentally, the wording of your question suggests that you think you may have more of a problem because the plasmid vector is a little larger than usual. Not so! Circularisation is favoured because the two ends are tethered so the effective concentration of each is high with respect to the other. As the plasmid gets bigger the tether is longer and the tethering effect will be less.

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


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What are the absolute facial features which features sexual dimorphism in humans?
Apart from beard and moustache, is there any facial feature that would help to distinguish between men and women?
It is said that men have square, rectangular or oblong face and women have oval,diamond or heart shaped face.
Also men are said to have thicker eyebrows, widely spaced eyes and prominent eyebrow ridges while women have longer eyelashes.
Again, men have wider mouth and women have fuller lips.And men have sharp jawline while women have rounder jawline.
This list can be extended further. However, there are several exceptions to the above mentioned generalization.
So,how can we instinctively determine biological sex(male or female) of someone just by looking at the face?

If you want to know how the brain 'instinctively' decides male or female you can go to https://cogsci.stackexchange.com/

@Roni Saiba How can I transfer this question to other StackExchange category? I want to know both about psychological aspect of recognizer and physiological characters of a person whose sex is to be recognized just by looking at facial features.

You can join the other stackexchange. I think moderators can transfer questions around so you can contact them in chat.


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Sorting beads with FACS
Does anyone know if it is possible to sort micro-beads, ideally magnetic, using FACS and if so what diameters can be sorted. I was thinking of using fluorescent beads that might help facilitate this but I have no previous experience with FACS.
Ultimately I want to separate beads into separate wells that can be used for PCR templates.
It would be helpful if anyone knows any studies that have used similar methods.
Cheers!

Just some questions to facilitate a good answer: What sorter do you have access to? Are they the MACS microbeads (Miltenyi GmbH)? What's bound to the beads?

I'm not sure what model the FACS is that I have access to, I can find out on Monday. We haven't decided what beads to use for our experiment yet, this is what I am trying to prepare. We want to isolate Bacteria and Archaea cells from environmental sediments but haven't decided the best way to do this yet either and what to use to bind the cells to the beads. These are all things that I'm currently considering but initially, most crucially, if it is not possible to sort beads using FACS then I will need to look for an alternative approach.

You can sort on a fluorescent signal, though I'd be apprehensive about sorting magnetic beads. The MACS microbeads are 50nm to start, which is probably below detection for sorters not sporting a 405nm small-particle detector, making a gating strategy using scatter difficult. Have you considered a negative magnetic sort where your flow-through is your population of interest, followed by FACS?

The reason I wanted to use magnetic beads is to isolate them easily from an environmental sediment sample, not to use MACS. Therefore I could use beads larger than 50nm, I've seen some available that are several microns in diameter. The beads would just be suspended in some buffer like PBS (or whatever is suitable for FACS). Ultimately I want to then separate these beads so that each is in its own well on a well-plate, I thought maybe FACS could do this?


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Ornithology related areas in Biology
In relation to my work, I'm looking at ornithology as a field, and it would be interesting for me to know which areas in biology relate to ornithology.
Any help is much appreciated!

Paleontology has paleo-ornithology as well, in fact dinosaur paleontology is very closely related.

First of all, you can look at the papers published in the Journal of the Avian Biology, the Journal of Ornithology and the Auk. There you can see how bright is the field. It is about conservation biology, distribution of species, ecology of species, behavior, migration etc.

An easy way to figure that out is to look at what ornithologists are actually doing.  If you look up the staff page for an ornithological institute, you'll be able to see what type of projects they're involved in.
Here is an example:  Percy FitzPatrick Institute of African Ornithology staff page


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What does "out-titration" mean?
I am reading an article on developmental biology and cannot understand (even after searching the internet) what is meant by "out-titration".
For example, in this phrase:

We have previously shown that Drf1, together with Cut5, Treslin and Recq4, are out-titrated on chromatin by increasing N/C ratios in vitro.

From this article: Chk1 Inhibition of the Replication Factor Drf1 Guarantees Cell-Cycle Elongation at the Xenopus laevis Mid-blastula Transition
Thank you!!

It does seem oddly phrased, but is still understandable. The paper explains how the combination of low zygotic transcription and increasing amount of DNA due to rapid cell division can function as a switch to trigger the mid-blastula transition. Before this event, most factors in the cell are of maternal origin (ie they are not being expressed in the zygote) and are thus in limited supply. As cell division progresses, the stoichiometric ratio between these factors and DNA decreases until, eventually, there is more DNA than these replication factors. At this point, you could say that the DNA has titrated the replication factors in that there is no unbound form left. This is analogous to the equivalence point of acid-base titrations commonly encountered in first-year chemistry courses.

Thank you for your input! I had correctly understood the general sense of the expression, but was wandering if it was a specific process.

@BeatriceBaldi No, it's just part of the description of the process described in the paper. I often say something is "titrated into/out of solution", which I believe is a more standard phrasing.


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what is the reason for using 70% alcohol (ethanol)l?
For the purpose of sterilization I am using 70% alcohol (ethanol) for a really very long time. but whenever I ask about why actually we are using 70% alcohol till now I did not get a very specific answer. So why actually are we using 70% alcohol for sterilization?

why use ethanol? or why use 70%?

You can probably switch to IPA, too, because it's cheaper. Also note that for disinfection alcohol works fine to blast vegetative microbes on surfaces but for effective eradication alcohol requires at least 60 seconds of wet contact time to really do its job!

accepted answer with a negative vote...interesting : first time to witness that scenario...

Alcohol and water both vaporize completely, leaving no residues. 70% ethanol has been found to be most effective in killing microbes. Higher or lower concentrations are not so effective in killing microbes.
As amir from the university of Karachi states:
70% percent of alcohol is ideal to a stronger solution. Pure alcohol coagulates protein in contact. Suppose the pure alcohol is poured over a single celled organism. The alcohol will go through the cell wall of the organism in all direction, coagulating the protein just inside the cell wall. The ring of the coagulated protein would then stop the alcohol from penetrating farther from the cell, and no more coagulation would take place. At this time the cell would become inactive but not dead. Under the favorable conditions the cell would then begin to function. If 70 percent of alcohol is poured to a single celled organism, the diluted alcohol also coagulates the protein, but at a slower rate, so that it penetrates all the way through the cell before coagulation can block it. Then the entire cell is coagulated and the organism dies.
https://www.researchgate.net/post/Why_is_70_ethanol_used_for_wiping_microbiological_working_areas [accessed Jul 14, 2017].
Martin Luther from Halle Witternburg states: The effectivity of ethanol as e.g. desinfectant or antiseptic agent depends on the concentration of ethanol-water-mixture: An ethanol percentage of 50-80% destroys the cell wall/membrane of bacteria by denaturing their proteins and dissolving their lipids (effective against most bacteria, fungi and some viruses; ineffective against bacterial spores). Therefore, the ethanol has to pass the bacterial membrane/wall to get into the bacteria - if you use 100% ethanol instead, the bacteria get 'sealed' and they will survive... An other mechanism is the high osmotic pressure of ethanol/water-mixtures; and the 70% has the highest one.
Here is an interesting experiment using alcohol water ratios:
https://www.youtube.com/watch?v=h3iUy4Wg8lg

you can perhaps try the alcohol-protein reaction by mixing it with an egg. a bit like some scotch whisky.

your answer was a little bit convincing but now i am thinking that which are the proteins which gets denatured and form the coagulation in the bacterial cell? these proteins are the plasma membrane proteins(extrinsic and intrinsic proteins) or the proteins in cytoplasm ?


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How does hypochlorous acid inactivate viruses?
I was reading how bleach was used very widely as a disinfecting agent during the 2014 West Africa ebola outbreak and am interested in the mechanisms with which hypochlorous acid inactivates viruses. Most of the studies I could find only focused on its activity against bacteria. I know viruses tend to be much more difficult to inactivate than cells as they're somewhat simpler and aren't really alive.

The other answer by @CMosychuk talks about the general aspect related to use of hypochlorous acid. I will discuss here its molecular mechanism of action.
Hypochlorous acid (HOCl) is a very powerful oxidizing agent. In aqueous solution, it dissociates into H+ and OCl- as:
$$\ce{HOCl \leftrightharpoons H^+ + OCl^-}$$
However, HOCl also destroys viruses by chlorination. It acts on anything, from lipids to nucleic acids. For example, Hawkins et al ,2002 describe in detail the effects of HOCl on nucleic acids. HOCl, by direct chlorination, leads to the formation of chloramines, and ultimately nitrogen-centered radicals. These radicals often react with each other to form dimers. Also, they have reported formation of single- as well as double-stranded breaks on application of HOCl on plasmid DNA. See this image:

These reactions render the nucleic acid useless and the virus harmless. In a similar manner, HOCl also reacts with polypeptides, ultimately leading to their fragmentation. See these images (from here):

Also, as mentioned in the other answer, application of HOCl has been shown to promote denaturation and aggregation of proteins. The linked paper also talks about HOCl's effects on other biomolecules, such as carbohydrates, but those effects would be out of scope here.

This one should be the accepted answer.

@ronisaiba haha thanks for appreciation! Its totally OP's choice which answer to select, and its all right if no answer is selected. After all, both answers are great in themselves, and selecting one answer should not mean that the second answer is useless :)

A 2008 paper in Cell elucidated a mechanism not far off from how heat-denatured proteins in a cooked egg aggregate, and never return to their native conformation (1).
Remember that proteins don't do their job outside of their native conformation. The hypochlorous acid post-translationally modifies the proteins in a way that they lose their shape and begin to aggregate. The authors believe that the reactions are sufficiently fast that the denatured product builds up faster than the refolding reaction can take place. Your innate immune cells do something similar to combat microbes or cells they recognize as distressed or foreign, known as oxidative burst, by releasing compounds such as hypochlorous acid.
Now, viruses are just protein coats and nucleic acid. Sometimes they have an envelope, but the envelope is typically quite easy to destroy with detergent. Naked viruses are known to be able to survive a number of days in harsh conditions. The virus depends on elements of the protein coat such as spikes to attach and facilitate entry into the host. Denaturing agents will act to destroy these structures, preventing infection.
So what are some important considerations?
1) Concentration: At an inappropiate concentration, common disinfectants will fail because they lose efficacy. For example, alcohols at least 65-70% abv are known to be the lowest efficacious concentration, and anything lower you see the killing begin to drop off. People tend to use bleach at 10% or 100ppm I believe.
2) Contact time: Proteins take time to denature and immediately cleaning away the bleach will not accomplish your goal. Five to ten minutes wet contact time is appropriate for bleach. If it dries it loses effectiveness. Anything higher you don't see an increase in effect, either.
3) Compound: Bleach isnt good for everything. It works on hard, non-porous surfaces, but it also requires pre-cleaning because without a detergent, bleach won't remove grime or films that may inhibit its action.

Wow, I didn't even notice that you were also writing an answer :P Anyways, +1!

Ah, can you see that sort of stuff? Thanks!


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Inheriting Modified DNA after CRISPR editing
If CRISPR is used to modify the DNA sequence to cure a disease - say MS in a woman - will the RNA guides also modify the sequence in her eggs so her children could be born without MS inherited from her.

First off, CRISPR can't be used to cure diseases in an adult human or, more generally, for any adult vertebrate at present.
As you can see in this paper, a major problem with CRISPR is it has to target specific cell types in tissues. As long as the targets are somatic and not germline, the edits made by CRISPR will not be heritable.


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Are my plasmids single-stranded?

Hi, in this agarose gel photo (70 volts, 3.5uL Gel Red in 30ml of TBE, 1% Agarose, 1 hour run), I've checked the digestion of a large plasmid (15Kbp, one cut site). The theory says that the digested plasmid (linearized) should migrate slower than the supercoiled form of the uncut one (bigger band of the Undigested Plasmid). In my case the digested plasmid is faster than the undigested one.
I've found that my digested plasmid could be single-stranded (http://bitesizebio.com/13524/how-to-identify-supercoils-nicks-and-circles-in-plasmid-preps/). Do you think that could be the case?

You assume that the undigested plasmid is supercoiled, but more probably it is in the relaxed circular form due to single strand nicks. This form migrates slower than linear DNA.

I think that the simplest explanation of what you are seeing is that the uncut plasmid is in the form of dimers formed by recombination between monomeric circles. These would be resolved into monomer-sized linear molecules in the digestion.
I haven't seen this idea of single-stranded circles before, but if it did happen then I don't think this form would be predominant, and of course such ssDNA circles would be unaffected by digestion.

In my opinion the undigested plasmid is ok, maybe during the digestion or after the plasmid became single-stranded.

Why would the plasmid spontaneously convert from dsDNA to ssDNA, in your opinion?

I don't think that the plasmid spontaneously convert to ssDNA, but maybe  I do something wrong, maybe something like pipetting too vigoursly? I don't know. My tutor says the band in the gel must be higher. I've done the cut 3-4 different times, also with a different enzyme but always the same result.


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Is there a database for immunoglobulin domain structure?
is there a database where I can find the sequences of the hypervariable domain of immunoglobulins and the sequences of the related antigens? Thank you

There are a number of databases that exist, though the one you would want to use will likely depend on what you need it for. The one that's recommended at my university is IgBlast, associated with The National Center for Biotechnology Information (NCBI), however I've seen IMGT as a recommended source, as well; it seems to have a wider array of tools. That being said, I can't say which you might find more beneficial, as I'm uncertain as to how you'd be using the resource.

essentially I am interested in the primary sequence of the variable regions of the immunoglobulins (let's say GALMF) and the corresponding antigenic primary sequence (let's say CHYR), this sort of association. Thank you, I will have a look at those databases.

actually, these databases are blasting tools to search for patterns. I am looking for a list of sequences hits with both TCR of Ig and related antigens, if any.


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Why do bad smells make us vomit?
According to my understanding, vomiting happens when the body wants to get rid of something that we have ingested or put in our mouths to get it out of the body.
So why is it that when something smells really bad our bodies make us vomit even if we have not ingested the food, or not even put it in our mouth yet? Is this something psychological?
Thanks!

If you have a concussion, your body decides that the costs of dropping your last meal are less than the risk of being poisoned, as it cannot decide where the side-effects of the concussion come from. I guess something similar is at work here.

The current hypothesis is anytime what your senses are telling you do not match your brain assumes you are hallucinating and thus want to get rid of as much of the toxic substance making you hallucinate as possible before it kills you.

It is not really making you vomit not directly, it is making you nauseous if you become too nauseous you vomit.(nausea has multiple triggers but for this I will stick to smell) Nausea exist to keep you from eating toxic food and to help you get rid of it if you do, the reflex is a balance between the biological cost of a meal(minimal) and the cost of being poisoned(extreme) so you can see why it might favor vomiting and losing a meal vs not vomiting and dying of poisoning than it would the two costs were not so drastically different.
Now your body can't really tell the difference between a smell coming from inside your mouth and one from outside, they both reach the nose by a roundabout course, and your mouth cannot smell. The closest your instincts can come is assuming a stronger scent is coming from the mouth since it is close and enclosed. That's why a stronger disgusting smell results in a stronger feeling of nausea. the stronger the smell the better the chance it is coming from inside your mouth.
Combine these two concepts and you can see how the stronger the smell and the more disgusting it is the more likely it is to make you nauseous it is the best protection our anatomy allows for. Now of course this is only the the current hypothesis, Nausea is not easy to study nor is it a in high demand for research.
Additional sources

"Now your body can't really tell the difference between a smell coming from inside your mouth and one from outside"
That would explain the question, but I really doubt that. At least, it needs more explanation. Maybe this would be worth another question that asks more of the details. As for me, I can clearly distinguish the reflex that makes me close my nostrils and run away for better air and what wakes me up at nights if there is something down in my stomach that needs to be thrown out.

If you need some bodily experience of what I'm taking, visit the nearest swear plant. The stench is unbearable if you hadn't had a chance of previous training. And it's only the smell. No real toxic compounds.

wakes you up at night is not being triggered by smell but by something else, like an illness. nausea does have multiple triggers.

waking up at nights for a smell of smoke had probably saved the live of millions of people. But what I think you are about to say, I said "what wakes me up at nights if there is something down in my stomach that needs to be thrown out", which matches exactly "like an illness. nausea does have multiple triggers"

@GyroGearloose - Studies have actually shown that very few humans wake up to the smell of smoke, and certainly not milllions. During sleep, the brain mostly turns off processing of smells (unlike sounds, touch, and light, for example. Hence the dire importance of smoke alarms.

@anongoodnurse me, at least, I do. In the past, and, good luck, hopefully in the future, too. Luckily, in the past it turned out to be only some overcooked (charred) food from some neighbor.

@anongoodnurse that would be neighbors in the same building, I don't have a dog's nose.

@anongoodnurse, another comment. Your smoke alarms are fairly restricted: they must not go off on cigarette smoke, and can't detect a smokeless fire that only is about to asphyxiate us with CO only.
Smoke detectors are surely a good thing, but they are not a talisman that wards off anything that includes all kinds of dangers from fire.

@GyroGearloose - I refer to scientific studies, not anecdote. Also, I mentioned the importance of smoke alarms for smoke, not the number of other things which you refer to. Maybe you believe smoke alarms are not so useful, but they, not our noses in sleep, save lives.

@anongoodnurse our talk gets into a private discussion. Consider opening a chat. I don't doubt that your smoke detectors can save lives. Alas, I have also negative experiences. At least on five occurrences they got off in my building (with 6 apartments) , and no-o-o-one except me made it out of bed to check if there relay was a fire. None of these was triggered by my nose, and none of theses had my nose feel anything, not even a cigar. Those alarms were not inside a specific apartment. What if they had been? Should I have been trespassing?


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Is Homo sapiens the only extant species of genus "Homo"?
Is Homo sapiens the only species of genus "Homo" that survived?

Yes, it is, but there is evidence that older species have cross-bread, and, in some sense of the word, have survived. The concept of a genus is not well defined.

Some people argue that given our close relatedness Chimpanzees and humans should share a genus, which would likely be the genus Homo, meaning Homo sapiens would be one of three species in that genus. But it's not the official classification.

Is Homo sapiens the only extant species of genus “Homo”?
Yes, Homo sapiens is the only species left in the genus Homo. To be more accurate, some even consider all modern humans as being part of the same subspecies Homo sapiens sapiens. In those terms, Homo sapiens sapiens is the only subspecies left in the genus Homo.
There were other lineages before though but they got extinct.
Other Homo lineages that existed
There were other Homo lineages that went extinct. Consider the followings for example

H. habilis
H. gautengensis
H. erectus
H. neanderthalensis (sometimes called H. sapiens neanderthalensis)
H. heidelbergensis

Related posts
Here are two other posts that may be of interest to you

Does it make sense to classify all humans in a single species?
How could humans have interbred with Neanderthals if we're a different species?


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Bootstrap values
What do the bootstrap values indicate about the relationship between the species? I'm working on Mega program but I don;t understand what bootstrap value means in simple terms and also what does it indicate about the relationship between species

Welcome to Biology.SE! What research have you done before asking it here?

The bootstrap values belong to a wide category of values called support values. Support values in general are used to give some indication of the degree to which one can be confident that the branch represents some "signal" present in the data.
In particular, bootstrap values indicate how robust the branches in the tree are, that is, how resistant they are to perturbation in the data. They are obtained by re-sampling columns in the data matrix, building trees from such re-sampled matrices, and looking at the proportion of the obtained trees that contain a given branch.
In the case of bootstrap, the re-sampling step is done the following way: Suppose that the original data matrix has N columns (i.e. N encoded characters, that can be nucleotides or amino-acids in an sequence alignment, morphological characters, presence-absence of genomic features, etc.). A new matrix will be obtained by randomly drawing one of these columns, N times. The new matrix will therefore have the same number of characters, but some from the original matrix will be present multiple times and some will be absent. This will influence the topology of the tree. For instance, if a branch was supported by characters that now are absent, this branch may not appear any more with this particular re-sampling. The re-sampling is usually done around 100 or 1000 times.
A low bootstrap value means that if the tree is built using a subset of the data, it is likely that this branch will not appear.
A high bootstrap value means that the branch will likely appear on a tree built from such a re-sampled matrix. This does not necessarily mean that the branch is more likely to represent the true historical relationships, though: sometimes, reconstruction artifacts can be robust. For instance, with some molecular phylogeny reconstruction methods, taxa may end up being grouped based on similarities in genome composition. High bootstrap values indicate that there is a strong signal in the data supporting the branch, be it historical signal or other.

Nice answer +1. Would you mind clarifying how we resample. Just explaining how are the data organized in the matrix might help to clarify what re-sampling columns in the data matrix really mean. Does it mean subsetting the SNPs sequenced, or the individuals available, or some other pre-processed statistics, etc...?

@Remi.b I tried to expand a little my answer. This is re-sampling of characters (conventionally encoded as columns), not individuals (conventionally encoded as lines). Note that re-sampling of individuals would lead to trees on different sets of taxa, and it would therefore be impossible to simply compare branches between trees and compute branch support values.

@Remi.b If you can read French and are interested in these support values thing, you may have a look at the introduction of my thesis (pages 9 and 10 of https://tel.archives-ouvertes.fr/tel-00331825/). I see that I mentioned "perturbations de l’échantillonnage taxinomique" in ways of measuring robustness, but I can't remember what I had in mind...

Wow I did not know people are still writing PhD thesis in french! It feels like a pain having to translate your publications from english to french just for the thesis. Yes, I can read french. Thanks for the link.

In France, I think it is still pretty common to write theses in French (especially in humanities, but not only). The main text of the thesis was written in French, but the articles were included as is, in English. I'm happy I could write in my mother tongue: it made the experience much more enjoyable.

Good. While french is my mother tongue, I personally always have a hard time to talk science in other language in english (which can arguably be a bit of a handicap for me). Where I am currently doing my PhD (at UBC, Vancouver, BC, Canada) the thesis is basically the publications copy-pasted together replacing in this article by in this chapter and writing a few words to make everything fit together so there is not much rewriting to do, that's why it feels like much work having to write the thesis in another language to me. Anyway... Cheers!


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Why similarities among organisms led scientists to believe that organisms are evolved?
Theory of evolution states that organisms are evolved into other more advanced ones over time because there are some traits in modern organisms resemble with organisms existing before (from fossil record). But it might be possible that each organism has created independently of each other. why similarities mean evolutionary relationship?

Theory of evolution states that organisms are evolved into other more advanced ones over time  Nope that's not what the theory of evolution is stating, mainly because the expression "more advanced" does not mean much and also is a loaded expression. You might want to start with an intro course to evolutionary biology to understand what the theory of evolution says. Understanding Evolution is a very introductory course you might like.

@Remi.b Alright I will have a look at what theory of evolution states but the basic thing is humans are thought to have evolved from chimpanzees. What I want to know is chimpanzees might resemble to humans but why chimpanzees are considered ancestor of humans? It might be possible that humans and chimpanzees created individually?

I answered this second comment in answer form as comments were too short for what I wanted to say

Approaching the question from the other direction, we understand how evolution could happen (similar mechanisms are used in e.g. computer genetic algorithms), and see some examples of ongoing evolution, like antibiotic resistance in bacteria.  But we don't see new creatures being created ab initio, and have no evidence for any mechanism by which they could be created.

I see you are new to stack exchange. If an answer states "not an answer" it might be a good idea not to mark it as best answer :) Nice question though!

@AksaK chimpanzee are NOT considered the ancestors of humans, they SHARE a common ancestor with humans, kind of how you and your cousin share an common ancestor. That ancestor is believed to look more like chimpanzee than us humans, but does not mean much.

@Clangorous Chimera: OTOH, there are some people here who mark perfectly good answers as "not an answer".

I will answer by explaining some misconceptions in your original question:

Theory of evolution states that organisms are evolved into other more advanced ones over time

Nope that's not what the theory of evolution is stating, mainly because the expression "more advanced" does not mean much and also is a loaded expression. You might want to start with an intro course to evolutionary biology to understand what the theory of evolution says. Understanding Evolution is a very introductory course you might like

@Remi.b Alright I will have a look at what theory of evolution states but the basic thing is humans are thought to have evolved from chimpanzees. What I want to know is chimpanzees might resemble to humans but why chimpanzees are considered ancestor of humans? It might be possible that humans and chimpanzees created individually?

No, the theory of evolution does not state that humans evolved from chimpanzees. It says that humans and chimpanzees / bonobos have a common ancestor (about 6 millions years ago) that was not a human, nor was it a chimpanzee or a bonobo.
You can find an introduction to phylogenetics in this post and you can find online tools to visualize the tree of life in this post.
Philosophical issue in your question
The theory of evolution makes predictions that have been tested and demonstrated correct. You are asking why would creationism would not lead to the same predictions. For this purpose, one need to know what predictions would creationism make but this is very much undefined. If you can point to specific predictions that creationism would make, then we could tell you whether we have a counter evidence. The issue is that there is always a way to say, everything has been designed so that it looks like evolution is at play even if species were created anew. But this is not falsifiable.
So, maybe you might want to make specific predictions, that in your opinion, would be congruent with creationism but not with the theory of evolution and then we can tell you if we have evidence to support this prediction.
Related posts
While it does not directly answer your question (because IMO, for semantic issue, the question is unanswerable), you might want to have a look at Is evolution a fact? and Demonstrable and repeatable examples of evolution

The main reason organisms not believed to be created independently, (besides no evidence for a creator to do creating) is that organisms do not just share similarities but they share similarities in a predictable pattern. Similarities are not random but follow a pattern that only makes sense if it is due to small changes over long periods of time in an ancestors/descendants branching tree of relationships. Two similar creatures will be equally similar to a third, and those three will be equally similar to a fourth and so on ans so forth in a nested pattern, not just a random assortment.
Humans might happen to be very similar to chimpanzees and vice versa by chance alone, but the chance of both humans and chimps also being very similar to gorilla is much less likely, them being similar in the same ways is even less likely, and the chance of all three also each being very similar to orangutan is even less likely, ect and so forth through the entirety of life. The chances of this arrangement of traits and genes happening by chance (aka without any actual relatedness or common origin) is so astronomically small it is difficult for us to even conceive of events that uniquely unlikely. There is a better chance of all your atoms happening to sync up so you fall/phase through your chair and plummet to the center of the earth in the next few minutes. In fact the entire field of Cladistics is about testing and mapping these relationships, and one of the things they constantly test against is a the possibility of an random or convergent assortment of trait.
This pattern also mirrors the pattern of human driven evolution (artificial selection) in which organisms are bred from other ancestral organisms through small changes by encouraging individuals with certain traits to reproduce and discouraging others, which at the time was far more well understood, which is how they recognized it. It is also why three chapters of Darwin's book was about show pigeon breeding.
And all that is before you get into things like the mathematical predictability of evolution, the fossil record, or directly observed evolution.

Another factor is that when we do see distantly-related organisms having a very similar appearance, we can often identify the evolutionary pressures that would lead to that similarity.  E.g. dolphins and ichthyosaurs look much the same because of hydrodynamics.


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Identify Huge Mystery Beetle
It is around 2 inches long, one inch wide, fat, hazel coloured with black specks and has short antennae. It's got a lot of cobwebs on its legs, since I found it in a corner in my house. It was found in North America.

Welcome to Biology.SE. Where in North America did you find it? Not the same species live in the Yukon than in the Yucatan. I edited the post to capitalize the first letters of your sentences and add the picture direclty in the post (which you can do with one of the icon above the content of the post when you click on 'edit').

It's a female Eastern Hercules beetle (Dynastes tityus). Unlike the male, the female doesn't have 'horns' as it doesn't need to fight in order to find a mating partner. It's the largest and heaviest beetle in North America. It belongs in Scarabaeidae or scarab beetles.

Source from BugGuide.com


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

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

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

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

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

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

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

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

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


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Does drinking dry water have same effect as drinking regular water?
Dry water consists of water droplets that have been coated with silica nanoparticles, which prevents the droplets from forming a liquid.
If a human swallows dry water, does it have the same effect as regular water? Or do the particles go through the digestive system without releasing water inside? Is it dangerous to "drink" dry water?

I suggest this question to be asked at the chemistry stack exchange.

Human health effects associated with silica exposure, especially crystalline silica (0.5–10 µm), have widely been studied. Occupational exposure to crystalline silica induces silicosis in workers (a fibrotic lung disease) and is also associated with lung cancer, emphysema, and pulmonary tuberculosis (Leung et al.
so im gonna say if you just straight inhaled silica nano-particles  it would be very harmful but would say that the nano-particles passing through you should not be a big factor (i would not drink it just because it could hypothetically go into your lungs

Welcome to Biology.SE. We're looking for answers that provide explanation, context, and include references to reliable sources. Don't give your opinion; explain why your answer is right with appropriate citations. Answers that don't include explanations may be removed especially when they don't address the question (inhalation ≠ drinking). Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then delete or [edit] your answer accordingly.

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


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Cerebral activity during exposure to non - visible light
Our eyes only have the ability to sense light within a certain spectrum. My understanding is that particular frequencies energize specific cells in our eyes, each responsible for a different "color". When these cells are energized, they each release an appropriate amount of their chemical transmitter to stimulate additional cells and create the perception of the object from which the photos originate.
At what point does this process not occur for non-visible light?
In other words, do we fail to see non visible light because our eyes lack the receptors for other frequencies, or does our brain receive signals that it just dumps because it has not developed to process the information?
Have there been any experiments done involving a brain scan while exposed to non visible light?

[D]o we fail to see non visible light because our eyes lack the receptors for other frequencies, or does our brain receive signals that it just dumps because it has not developed to process the information?

It is because our eyes lack the receptors for other frequencies.
Humans have 3 'color receptor' called cone cells. We have three types of cone cells, each sensitive to a specific range of wavelengths. Here is a diagram of the sensitivity of each of these three types of cone cells.

As you can see, we do not have receptors for wavelength below 390 nm or above 700 nm which is our visible spectrum.

Awesome, thanks. I guess I was kind of hoping for some hidden brain activity  :-D

Vision is based on a protein interaction with a molecule called retinal from vitamin A.
Wavelengths of light in the visual range cause a photoisomerization of retinal (a cis- to trans- change), which is sensed by the protein that is "holding on" to the retinal.
Wavelengths that do not cause this photoisomerization cannot be sensed by the photoreceptors of the retina, so there isn't any signal produced to transmit to the brain.
However, there is some filtering done by the lens of the eye. Without the lens, humans (and other animals) can see further into the UV range. That UV light is also damaging to the retina, though, so it's best to keep the lens intact.
Note that the image in the answer by @Remi.b is actually from a psychometric experiment, so the lens is intact. The responses there are actually human perceptual sensitivity to light for each cone. The blue curve would go off to the left quite a bit further into the 300nm range if the lens were not present. The research subjects probably prefer the experiment as-is, however.
You wouldn't perceive that UV light much differently than a far violet color, however, because differences between different cones are necessary for color vision, and by that end of the spectrum only the cones responsive to the shortest wavelengths are responsive at all.

Of course, we do detect infrared and ultraviolet light in a sense. We feel infrared (heat) and UV can cause skin issues. You could say that the brain detects this, but you can't make out the form of an emitting source.

@JackR.Woods Those are completely different processes from vision. Chemically, sensing heat and UV are totally different from the processes that occur to detect visible light in the retina.


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What determines the courses of multi-dose vaccines?
I understand that some proportion of individuals will fail to develop immunity from a single dose of a vaccine.  Rather than test every member of the target population following each vaccination, it is more economical to administer multiple doses to increase the population immunity rate.
But what determines how many doses are indicated for a particular vaccine, and how widely they are spaced?  Are these variables rigorously optimized, or are they just accepted heuristics?
E.g., two doses of MMR are indicated, separated by at least 3 years.  Three doses of HPV are indicated, separated by 2 and then 3 months.  Four doses of IPV are recommended, as are five doses of DTaP!

Have you done any research into this? It would seem to be easy to Google. Please share what you found and why this doesn't answer your question.

@anongoodnurse: Best I could find was this, which describes different immunological mechanisms, but which does not answer this quesiton.  Also, this explaining that it's always cheaper to add another dose than to titrate a sample from an individual to determine their acquired immunity.

You should be editing this information into your question. :)


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Were Telomeres the Master Key to Abiogenesis
Knowing as we do now that all manner of complex organic molecules and viscelles/micelles form spontaneously in various environments, from hot vents perfect for basic hydrophobic H-C fatty acids and stable charged H-C-O-P hydrophobics - to volcanic glass micro-chambers, clay-layer geometry and water ice fractal symetry,  that all combine to create ideal nanoscale everywhere rapid self assembly scenarios for various amino acids etc that in turn can form RNA like segments and combinations... I can't help but wonder what scenario is best situation pre-biotic that can form Telomeric sequences.
It seems to me, an instinctive feeling after viewing so many bioscience and life origin videos, that in all the random prebiotic assembly and disassembly of molecules, the perfection of replication lies in repetition that first needed a master start and stop sequence control, as master of other sub gene start stop codons.
Of course a myriad of biophysics factors come into play in origin theory and I am far from expert but I wonder if anyone can provide solid
references about abiogenisis and telomeres?
Tough question to word here, and too vast a topic when I try and narrow the web searches.  However, the amino squences for telomeres are finite I believe and so before life kept repeating itself what molecules in what environment crates the combination best?

When you refer to amino acids (twice) I assume that you mean nucleotides?

I believe that is correct Alan. Being uncertain I used the word amino sequence, although that might be ambigous.

This lecture discussing the crebs cycle, along  with a beautiful animation illustrating the natural harmony of sequential assembly and disassembly  of H C and O building blocks, maybe be more the answer to my phrase "Master Key"  https://youtu.be/0cwvj0XBKlE?t=41m16s

No, they weren't. Interesting hypothesis though!
However, that hypothesis is missing a very important piece of information: prokaryotes don't typically have telomeres.
Because their DNA is typically circular, rather than linear, telomeres aren't necessary, and there is no shortening problem.
See the Wikipedia page on telomeres for more information. There are various theories on the origins of telomerases and telomere evolution, check out Google Scholar.


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Are 'homeothermic' and 'endothermic' synonymous?
I got this question from the comments below this answer. So, do homeothermic and poikilothermic have the same meaning as endothermic and ectothermic, respectively?
 A user also suggested that the terms such as poikilothermic and homeothermic have become obsolete. What is the reason for them being obsolete?

[D]o homeothermic and poikilothermic have the same meaning as endothermic and ectothermic respectively[?]

No. Once you are referring to the source of the heat, while the other time you are referring to whether the internal temperature varies through time.
Source of heat

endo = inside
exo = outside

Variance in internal temperature

Poikilo = varies
homeo = does not vary

Combinations
Any combination of these two axes exist. For example: If the temperature in the environment never varies you can be homeotherm without needing to be endotherm. You, for example, are a homeo-endo-therm.
A fun common example are the large dinosaurs that are thought to be homeotherms (but see @John's and @Gerardo's comments) because their metabolism produce some heat as by-product (just like any organism) and they are so large that they remain warm thanks to this heat source. However, they were probably not able to regulate actively their temperature. Therefore, I would tend to qualify dinosaurs as homeo-exo-therm but I wouldn't be surprised if someone prefers to call large dinosaurs homeo-endo-therm.
Note that the terminology might be a bit more complicated in reality as the diversity of mechanisms of body temperature regulation is important.

The whole mass-homeothermy thing tends to only pop up from people who don't understand dinosaur anatomy, larger dinosaurs are not going retain significantly more heat than elephant sized dinosaurs, and no one would argue elephants are homeoectotherms.  Long necks, long tails and  widespread air sacs provide gigantic heat exchange surfaces.

There is little doubt that the extinct dinosaurs were thermoregulators. The question is if they were endotherm thermoregulators or ectotherm thermoregulators. At least one group of dinosaurs (birds) is clearly made of endotherm thermoregulators. The modern consensus is that most of them were something intermediate, called mesotherms

Traditionally, the terms poikilotherm and homeotherm were used to refer to organisms that don't regulate their body temperature and that regulate their body temperature, respectively.
However, those terms are not the best ones, regarding their etymology. For instance, poikilos (Greek ποικίλος, "many-coloured") means "diverse", "varied", while homoios (Greek ὅμοιoς) means "similar", "resembling". But some fish, which we define as a poikilotherm, may have a lifetime body temperature variation of 1℃ or less, while some mammals like a squirrel, which we define as an homeotherm, may have a daily body temperature variation of more than 20℃.
Then the terms ectotherms and endotherms appeared, as a new and modern terminology. And they are indeed meant to be that.
The problem is that a lot of people simply thought that ectotherm was a new name for poikilotherm and that endotherm was a new name for homeotherm, as if they were synonyms. But they are not. Follow me:
(A word of caution before we proceed: unfortunately, there is no organisation that regulates the terms used in the various branches of biology, as IUPAC does for chemistry. Thus, the acceptance of a term depends largely on the consensus among the researchers and the book authors. My answer here describes the nomenclature used by Whithers, Comparative animal physiology, in my opinion the best book on comparative physiology.)
Thermoconforms and Thermoregulators
According to Withers (1992), animals can be classified in two groups, regarding the ability to regulate their body temperature:

Thermoconforms: animals that don't regulate their body temperatures. Their body temperature is pretty much the temperature of their surroundings.
Thermoregulators: animals that actively regulate their body temperature. Their body temperature, therefore, may differ from the temperature of their surroundings.

In Withers' words:

Most animals are unable to control their body temperature, and Tb passively conforms to their thermal environment; these animals thermoconform [...] Some animals, in contrast, regulate their body temperature often against a substantial thermal gradient between their body and the environment; they thermoregulate.

By the way, this suffix pattern of _conform and _regulator is common along the book. For instance, Withers talks about osmoconforms and osmoregulators (capable or not of regulating their body osmolarity), and so on.
So, thermoconform and thermoregulator are terms that describe if the animal is capable or not of regulating its body temperature. But those terms do not describe the source of the thermal energy.
Endotherms and Ectotherms
Here comes endotherm and ectotherm. In short:

Endotherm: the main source of heat (thermal energy) is the organism itself.
Ectotherm: the main source of heat (thermal energy) is the environment.

According to Withers:

The terms ectotherm and endotherm are perhaps the most useful for describing the thermal capabilities of animals because they have a mechanistic basis. An ectotherm is an animal whose thermal balance is predominated by external sources of heat, and its metabolic heat production is insignificant. [...] Endotherms are animals whose thermal balance is predominated by their endogenous metabolic heat production.

Now we can try to combine those terms, and that will led us to the comprehension that none of them is synonymous neither of poikilotherm nor homeotherm:
All thermoconforms are ectotherms, that's not problematic. But things become complicated when it come to thermoregulators: thermoregulators can be ectotherms or endotherms.
For instance, most reptiles are ectotherm thermoregulators, but some dinosaurian reptiles, such as the birds (and most probably all other Dinosauria), are endotherm thermoregulators.
This table (ibid) summarizes the possible combinations very well:

Conclusion
It's clear that the terms poikilotherm and homeotherm (or even worse, cold-blooded and warm-blooded) are outdated and inadequate.
But they should not be simply replaced by the pair ectotherm/endotherm. Ectotherm and endotherm are terms that refer only to the main source of heat. The most adequate terms for describing the ability to regulate the temperature are thermoconform and thermoregulator (which, by the way, are not synonymous with poikilotherm/homeotherm either).
Source:

Withers, P. (1992). Comparative animal physiology. Forth Worth: Saunders.


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Renorenal Reflex
According to this:

The kidney contains afferent sensory nerve fibers that are located primarily in the renal pelvic wall where they sense stretch.

I think the stretch is due to urine. If I am correct then, I am unable to understand the following:

Stretch activation of these afferent sensory nerve fibers elicits an inhibitory renorenal reflex response wherein the contralateral kidney exhibits a compensatory natriuresis and diuresis due to diminished efferent renal sympathetic nerve activity.
  There is a negative feedback loop in which efferent renal sympathetic nerve activity facilitates increases in afferent renal nerve activity that in turn inhibit efferent renal sympathetic nerve activity so as to avoid excess renal sodium retention.

If I am correct , then how is renorenal reflex a negative feedback loop? Doesn't decreased efferent sympathetic activity increasing diuresis thus causing further increase in pressure in renal pelvis( contra lateral)?
Also how is sympathetic activity increasing renal pelvic pressure in the first place?
If I am wrong then, what is causing increase in renal pelvic pressure?

Support for my claim:
Hydronephrosis, a blockage of the outflow of urine or reverse flow of urine already in the bladder (called reflux) can cause the renal pelvis to become enlarged.
So, I think I am right in saying that urine increases pressure in renal pelvis, thus activating stretch receptors.

Chapter 8 from the book Neural Control of Renal Function has all the explanations you need: https://www.ncbi.nlm.nih.gov/books/NBK57250/

Unfortunately, I am still confused, please give a hint.

How is renorenal reflex a negative feedback loop?

You are confusing two different negative feedback loops.

1) There is a negative feedback loop in which efferent renal sympathetic nerve activity facilitates increases in afferent renal nerve activity that in turn inhibit efferent renal sympathetic nerve activity so as to avoid excess renal sodium retention.

This occurs on ipsilateral kidney only and is not renorenal reflex.

2) Stretch activation of these afferent sensory nerve fibers elicits an inhibitory renorenal reflex response wherein the contralateral kidney exhibits a compensatory natriuresis and diuresis due to diminished efferent renal sympathetic nerve activity. The renorenal reflex coordinates the excretory function of the two kidneys so as to facilitate homeostatic regulation of sodium and water balance.

This is renorenal reflex, while it is negative feedback again, since reduced urine passage in one kidney paves way for other to increase urine passage/output.

Doesn't decreased efferent sympathetic activity increasing diuresis thus causing further increase in pressure in renal pelvis( contra lateral)?

Contra lateral kidney is not having same renal obstruction as in ipsilateral(unless otherwise stated). So, diuresis leads to increased loss of loads of electrolytes and water, thus, reducing hypertension.

Also how is sympathetic activity increasing renal pelvic pressure in the first place?
  If I am wrong then, what is causing increase in renal pelvic pressure?

Sympathetic activity is not increasing renal pelvic pressure here. Increased renal pelvic pressure was caused by obstruction to urine flow, eg. ureteral caliculi. Due to this obstruction urine could not pass from pelvis to bladder which increase pelvic pressure.
Contrarily, increased sympathetic activity in ipsilateral kidney tends to reduce pelvic pressure by reducing GFR. In contralateral kidney, decreased sympathetic activity will cause increased diuresis and reduced tension on diseased kidney for urine output.
Note: Increased GFR here, as a result of decreased symp supply, does not cause increased renal pelvic pressure since urinary passage is clear and not obstructed.

No, I don't no how is sympathetic activity increasing pressure in renal pelvis, asaik sympathetic activity will reduce gfr so reduced pressure in the renal pelvis.

Refer to edited answer.


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What is the difference between "dysregulation" and "deregulation" of miRNA?
I've started to study the role of miRNA in cancer. Wikipedia says:

Just as miRNA is involved in the normal functioning of eukaryotic
  cells, so has dysregulation of miRNA been associated with disease.
The first human disease known to be associated with miRNA deregulation
  was chronic lymphocytic leukemia.

1- What is the difference between dysregulation and deregulation?
2- How are these concepts related to RNA degradation?

This is not a homework question but a badly researched. These questions should not be closed as homework (as this is misuse of this reason), but downvoted + commented. The downvotes can be reversed if the question is edited.

Here at biology we expect people who ask questions to do some research by themselves. What have you found out?

@Chris — I appreciate your good intentions acting as moderator here. However, the ‘close category, ‘homework’, clearly includes “A question that addresses a basic biology concept that may seem trivial to biology professionals”. (And there is a review category allowing one to vote to close “Low quality posts”.) I have posted on meta about this being unsatisfactory, and feel that discussion — on meta — is required (as a separate question) on how to resolve this unsatisfactory situation.


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In plants why are potassium and nitrate ions absorbed faster than any others?
Quoting my A-level biology textbook:

$\ce{K^+,  NO3^-}$ are absorbed by plants faster than any other ions. Whereas, $\ce{Ca^2+, SO4^2-}$ are absorbed with the slowest speed.

What is the reason?
My reasoning: I first though the size of ions would matter in this case. Obviously, $\ce{K^+}$ is smaller than $\ce{Ca^2+}$,  then it 'seemed to me' that smaller ions would be absorbed faster. The same reasoning can be applied to $\ce{NO3^-,  SO4^2-}$. But, there are smaller ions than $\ce{K^+}$ which are absorbed slower eg. $\ce{Na+}$. So, obviously size only does not matter here. There are other factors.

What reasons has your own research uncovered?

@James See my edit.

Since plants absorb minerals, like potassium, calcium, sulfur, etc. in their ionic form, like K+, NO3-, SO42-, Ca2+, they need to absorb them actively. Since these ions are charged, they have difficulty while passing through the plasma membrane. Hence, plants need to expend energy in order to transport them. For this, they use ATP and membrane transporter proteins. These transporters transport ions across cell membrane with an accompanying ion (H+) so as to maintain electrochemical gradient. As a result (partly), these transporters are highly selective for the ions they carry. For example, a K+ transporter will not transport SO42- or another ion. See this answer to see how transporters achieve this selectivity.
The above part explains how ions are transported in plants. Now, lets come to the main question i.e. why some ions are transported faster than others. Well, there is no definitive answer to this (at least none that I know of). But I can think of two possible reasons for this (using only the examples of K+, Ca2+, NO3- and SO42-):

Magnitude of Charge: one fact here is that both K+ and NO3- have a charge of $\pm$1, whereas Ca2+ and SO42- have a charge of $\pm$2. So what? This makes their transport a bit more difficult. For example, to transport K+ across the membrane, the transporter would antiport 1 H+ for 1 K+, whereas a similar antiporter would transport 2 H+ out to bring 1 Ca2+ in. Obviously, this does not explain the difference between ions with same charge, which the following point seems to do.
Requirement: one of the most important points to keep in mind here is the difference in requirements of different ions by the plant. This is why plant macronutrients (i.e. required in large quantities) have been divided into primary macronutrients (N, P, K) and secondary macronutrients (all others, including Ca, S, Na). As you see, nitrogen and potassium are mostly the limiting factors of crop production. This is why plants require them in large quantities, and hence try to absorb them as fast as possible. This, partly again, explains why K+ and NO3- (the only artificial nitrogen source other than NH4+) are absorbed faster by plants while Ca2+ and SO42- are absorbed slowly.

References:

Mineral Absorption - Wikipedia
Secondary Plant Nutrients: Calcium, Magnesium, and Sulfur - Mississippi State University

Great Answer. I will for some time before selecting it


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Neurons competing for survival
I was reading in a book that in the process of neurogenesis - when new neurons are born -  neurons compete for survival. Or in other words they have to make themselves useful to the brain otherwise they die and become processed as brain food.
To what extent is this real and how often does this happen?
i think that in the book I was reading it the author mentions it happening in early life, but I'm not entirely sure.
Would be great to know.
Thank you!

Welcome to Biology.SE and thanks for your question. Could you please provide a reference to the book you've read this in (and a direct quote of the claim would also be much appreciated). Thanks!

It's definitely real ;)
Depending on your previous knowledge, this review from 1987 might be a good starting point.
http://science.sciencemag.org/content/237/4819/1154.long
To give you an idea of recent developments this article is an easy read. Be sure to browse the references.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/

Welcome to Biology.SE! Could you include some relevant text from your sources, both for ease of reading and in case those links die?


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What is this plant with some seeds around its leaf?
I am in India, This plant is growing on floor with very less soil
on it. I took 3 pictures of the same plant, It just rained yesterday.
I didn't see any insects around this plant. here is it:

Third picture is this: http://i.imgur.com/vxxCJos.jpg

It is Andrographis paniculata also know as Kalmegh or Kalamegha

It has close resemblance to Mexican Tea Plant also.


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What happens when you tag a protease with its own degradation tag?
I've been learning about the ClipXP, ClipAP, and Lon proteases. They are proteases from the AAA+ family, which seek out proteins tagged with certain peptide sequences, unfold them, and chop them up.
But what happens when you tag a protease with its own degradation tag? For example, what if you took DNA encoding mf-Lon and added its ssrA tag to the end, and then expressed this sequence in bacteria?
Would this result in any interesting dynamics? Will the protease start trying to degrade itself like an Ouroboros? Will it get stuck trying to do so? Will we observe any interesting dynamics when we incorporate this into a gene circuit?

The proteases would presumably degrade each other.

Yeah @canadianer. But I wonder if anything would be different from normal protein degradation. Maybe the protease concentration may have a lower and perhaps more stable steady state? Perhaps because the protease is evolved to degrade other protein, it might be more tightly folded and hence harder to degrade? Might it even get stuck trying to do so? what if two proteases bite each other 69 style?

You may be dealing with an example of autocatalysis and this may give rise to an S-shaped progress curve (that is, an S-shaped velocity-vs-time plot; not to be confused with an S-shaped velocity-vs-substrate plot). A very good example is trypsinogen/trypsin.  See Fig 2 of  ISOLATION FROM BEEF PANCREAS OF CRYSTALLINE TRYPSINOGEN ... by Kunitz and Northrop (pdf is free).  The kinetics of such a system is well treated by Frost and Pearson, p19

The process of self-degradation of a protease is called autolysis, and the rate of autolysis depends on many factors including temperature, pH, and enzyme concentration.1,2 While most proteases show reduced proteolytic activity with increased autolysis, some proteases demonstrate increased activity after they are self-hydrolyzed. The most notable example is trypsinogen, which, when cleaved initially by enteropeptidase, yields trypsin, an important digestive enzyme. Trypsin can then hydrolyze more trypsinogen molecules in a process known as autocatalysis / autoactivation.3

References

Chen XL, Shun CY, Zhang YZ, Gao PJ. Rapid monitoring of autolysis process of proteases by capillary electrophoresis. Biotechnol Lett. 2003 Oct;25(20):1763-7.
Khalil ME, Metwalli SM, El-Sebaiy LM. Factors affecting the autolysis rate of crude preparations of proteolytic enzymes from Bouri fish (Mugil cephalus). Food Chem. 1987, 24, 127-135.
Mayer J, Rau B, Schoenberg MH, Beger HG. Mechanism and role of trypsinogen activation in acute pancreatitis. Hepatogastroenterology. 1999 Sep-Oct;46(29):2757-63.


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Are there hyoid bones of Homo habilis in the fossil record?
Hyoid bones have been found for Homo erectus, Homo neanderthalensis, Australopithecus afarensis, and some more hominids. Have hyoid bones been found from Homo habilis?

References:
Capasso, L., E Michetti., & R, D'Anastasio. (2009). A Homo Erectus Hyoid Bone: Possible Implications for the Origin of the Human Capability for Speech. Coll. Antropo. 32(4), 1007–1011
Alemseged, Z., Spoor, F., Kimbel, W. H., Bobe, R., Geraads, D., Reed, D., & Wynn, J. G. (2006). A juvenile early hominin skeleton from Dikika, Ethiopia. Nature, 443(7109), 296-301.
Steele, J., Clegg, M., & Martelli, S. (2013). Comparative morphology of the hominin and african ape hyoid bone, a possible marker of the evolution of speech. Human biology, 85(5), 639-672.


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What is the function of multiple nuclei in syncytial cells?
What is the function of multiple nuclei in syncytial cells specially in protists with cilia? Is multiple nuclei a special characteristics of only ciliated cells?

A mononucleate's size is limited by its nucleocytoplasmic ratio, and protozoa like being big.
The solution? Multiple copies of the same genes in huge nuclei, or multiple individual nuclei.
Multiple nuclei are common in any large, complex cell. There is nothing specific to the presence of cilia that require multiple nuclei, and ciliates are not the only multinucleate protozoa (the amoeboid Chaos genus can contain up to a thousand). The reason large, complex cells require this is simply because they are so big. Such a huge size requires, in addition to more complex nuclear regulation, a high total protein turnover, which in turn requires a high transcription rate. Even with mRNA being translated by numerous ribosomes, the amplification factor is still limited. Having multiple nuclei increases the rate of mRNA production, which increases the total synthetic capacity of the organism. When only a specific gene is required to be transcribed at a high rate, that individual gene may be duplicated many times. This is often seen in the nucleolus, which contains many copies of the same genetic material required to create the huge amount rRNA needed for ribosome biosynthesis:

Many protozoa are large because they are packing as much complexity into a single cell as they can, even to the point of having a backbone-like structure or simple photosensitive "eyes" (though not all protozoa are large). Many adaptions are required to allow single-celled organisms to grow to this size, such as a more complex cytoskeleton, a dedicated feeding apparatus, a contractile vacuole, etc. Multiple copies of genetic material is just another required adaptation. This adaption can manifest itself in various ways. Some organisms have multiple copies of the same nucleus. Others fuse these nuclei into a single, large nucleus (a macronucleus), keeping a limited number of micronuclei around for sexual reproduction:

Multicellular organisms tend to have multiple nuclei in specific cells for the same reason. Many types of cells, for example, require an extremely high rate of protein turnover and are very large (such as skeletal muscles), so they have multiple nuclei. This occurs when a single nucleus is no longer sufficient, even at peak capacity.
I would like to point out that what you are describing is a coenocyte. A syncytium is a multinucleated cell which has arisen from the fusion of multiple cells and their constituent nuclei (karyogamy), whereas a coenocyte is a cell which had undergone multiple rounds of nuclear division, without accompanying cytokinesis.

Regarding your second question:
Multiple nuclei in a single "cell" is not exclusive to ciliated cells.
Muscle fibers of animals or placenta of mammals undergo cell fusion, resulting in multiple nuclei in one "cell".
Embryos of some animals start with nuclei division without cell division, also resulting (temporarily) in multiple nuclei in one "cell".
Other examples are provided here: https://en.wikipedia.org/wiki/Syncytium


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Explaining a branch with visibly different leaves on Citrus japonica
My father was so kind as to send me a tree of Citrus japonica, aka Fortunella japonica aka kumquat (all names mean the same according to Wikipedia). Though I have seen this species many times, it is only now that I noticed two very distinct kinds of leaves.
One kind of leaves that I call  'double leaf' (second image) is only found on one single branch. The branch is still green down to where it merges with the tree, but many of the leaves are among the biggest on the tree. Excepting one sickly not fully formed leaf, all leaves on this branch seem to be of this 'double' type. I checked carefully.

All other leaves are of the kind shown in the first image.

This is the tree as a whole:

How can this different type of leaves on just one branch be understood? Does that branch belong to a different kind of Citrus (meaning grafting occurred), or is this a stage in leaf development? I don't think the latter, because I found small single leaves in the top branches of the tree. But I also don't think the former, because father said no such thing. If it is a mutation, why does it solely affect one branch?
I am a particularly ignorant amateur, but if you instruct me what to observe or photograph, I shall gladly do so.
Edit:
I thought I should supply a picture of where the unique branch emerges from the tree:

The tree bears fruit and at its thickest point is marginally thinner than my thumb.
Edit:
It just occurred to me that the entire upper kumquat might be grafted onto a different kind of citrus, which would explain such behaviour in the lower branch. I will search for evidence of this in the morning.

You are interested in developmental biology.

@SANBIsamples I am a layman with very little knowledge about biology. I think you are saying it is a mutation. Why does it appear in this branch only?

Don't worry @Ludi, I'm not British. You don't have to say you're a layman at the onset or even play humble :) A mutation can appear whenever cell division goes wrong. Yes, it's probably a mutation.

It was probably a graft onto another citrus rootstock, so you might get shoots of either types of citrus

What you are seeing here is an example of a winged petiole. The petiole is the leaf stalk and these can have wings called stipules.
According to this source kumquat leaves have narrow petioles. I can't explain why you are seeing variation on a single plant, but I recall seeing similar variation on garden citrus in California, so I suspect it isn't unusual.


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Is it possible to build a hive for bumblebee or hornet
People commonly build hives for honey bees and it works . Is it also possible to build a hive for a bumblebees or hornets ? Should it have any special shape or form or is it just impossible ?

Yes, it is very common practice and there are many instructions and plans for beehives/nests available online, there are some for wasps


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Identifying very tiny worm
i couldn't take a picture because i get rid from it as soon as posible. Because i thought maybe it was a bad parasite.
But i draw a picture of it at my computer. But my picture not very accurate because it was very tiny to see what it actually look like. and i cant remember all of the characteristics of it.
It is very tiny about 5 mm in length. and maybe almost 0.1 mm thick. I assume that yellow thing is head, because of movement directions is towards that way. To move, he elongates its own body then holds to surface with its own head, then let free its other ends grasp from the surface simultaneously shrinks to shorter length maybe half of its elongated length. than repeats whole process.
It was shrinks and elongates to move
it was moving like its got very soft body. and it was becoming significantly thinner when elongates.
Sometimes looks like checking surrounding surface with his head. Seem like it tries to navigate.
finally I must describe how my picture could inaccurate: it was very tiny i cant see his body parts exactly. i guess i see a tiny structures appears like his 2 pair back leg and 1 structure ball like thing attached to end. But this structures possible thickness are micrometers so i also thought that structures could be attached dust particles. And i also saw structures like this at the front end, but it was so tiny, i cant even drew because i see just barely but cant figured what was it like.
only im sure about its head and white-ish neck.
it is elongated at the picture.
So picture is representing what i see. but not %100 accurate. due to reasons i described.
i hope my questions description is enough and isn't improper.

I think without an actual picture it's going to be nearly impossible to identify. Species identification is very difficult and often depends on details that aren't initially important. But I can tell you that if it has legs, it is not a worm.

@BryanKrause yes imposible but i was hoping to get a general idea like a family or genus guess rather than exact specie.

Interesting question, and probably a little bit hopeless. I don't see how anyone could give an answer without a lot if guessing. Maybe you should remove the inchworm image, since that just seems confusing if it wasn't really "inching". As @BryanKrause says, it's not a worm if there ar legs. But a lot if insects have larva that are a bit worm-like. Maybe try googling videos of different larvas? I'm guessing fly larva of some sort. How does this hover fly larva look? https://www.youtube.com/watch?v=gkU8YHpuAtw

@picapica now i watched this video and it is so close what i see, especially about movement type. But my things was more thinner at the body. Tomorrow ill google about relatives of Hover fly, thanks for the video.

Was it an inchworm? It fits the description, as well as the 2nd picture.

no. sorry i guess i didnt clearly asked. 2nd picture doesnt represents it. 2nd picture just here to describe how it moves. thanks for answering.

1st picture is represents it with high but limited accuracy.

but maybe it is very far relative of inchworm. but two things doesnt fit to inchworm. Inchworms body is too bigger than it.and mainly inchworm bends  not shrinks like what i see.


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What is the name of this fly?
I've seen the following insect in Austria at the border to Bavaria (high resolution). It was quite small. I would guess not longer than 1cm:

Could somebody identify it?

Type of robber fly perhaps?

Not a robber fly; I think Empididae; doing a search on https://diptera.info/infusions/aw_forum_panel/search.php for that family name might suggest a deeper identification

@GerardoFurtado Thank you :-) I like taking close-ups and this one was a lucky one. I almost touched the insect with my camera lens but it didn't move. A really professional photo model; I wish more insects were like this ;-) And usually I put those photographs under CC0 on Wikipedia Commons to make it easy to use them.

yes, definitely Empididae with that long "snout". (but i can't be more precise than that.) i've also notices that a lot of them seem to be nice and slow!

Could somebody identify it?

Sure, I'd be glad to help you with that!
The fly in question is indeed a member of the Empididae family, and of the genus Empis. I couldn't quite decide on the species, but it's either Tessellata or Opaca (with me leaning more towards Tessellata). This fly (genus) is commonly referred to as a "Dance Fly".

Empis Tessellata

Empis Opaca


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What is this thorny plant with cute leaves?
I found this thorny plant with cute leaves growing in my garden in India,
I took a risk by plucking it to get photos of the front & back side of the leaves.
Front side of the leaf:

Back side of leaf:

Full plant:

Any Idea what this plant is?

Full Plant: http://i.imgur.com/0IlEj2G.jpg

https://en.wikipedia.org/wiki/Dalbergia_melanoxylon
The Mpingo looks quite similar to this plant. However, more information is needed like the approximate size of the leaves and the number of leaves on a branch.

No, That is a wrong answer.


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Do smaller intelligent animals have a higher neuron density to account for their seeming intelligence? Otherwise, what?
It seems like there's a lot of very small animals that have a much higher intelligence than what you would expect if you linearly projected intelligence as a function of brain size. There's ravens, crows and parrots which are much smaller than humans but have a recognizably high intelligence and emotional capacity. Then there's rats and general rodents like squirrels or similar animals like raccoons, and I guess an octopus to throw in which are good at problem solving and fierce fighters. Then there's also bugs like ants which are somehow very versatile and can adapt to many situations despite being that tiny, and with recent information may also have a recognizable emotional capacity like possibly bees.
It would make sense to me if the correlation between neuron density and intelligence isn't linear, but I don't have the information to make any determinations.

@Remi.b You might also consider this and this.

I think the major challenge here is defining "intelligence" in a comparative way. You give many examples which could in their own way be described as intelligence. A better question would be to start with scaling of neuron density across animals. Then get to the question of complexity of behavior.

I mean I asked about neuron density, but for some reason people keep diverting to other points.

@Remi.b - Questions shouldnt be closed if fit for CogSci and Bio. They should be closed if unfit for Bio.

@AliceD Yes, in the post I linked from the meta site (here), I expressed my opinion that CogSci type of question should be off-topic on Bio.SE but as few seem to share this opinion, I happily follow the majority. I retracted my close vote but forgot remove my comment. I will remove my comment now. Thanks

IMO, this question is primarily opinion based, due to no efforts being made to actually define "intelligence". Instead, only casual & extremely broad scoped, surface-level examples were mentioned. Also, I believe any answer will be either too broad, or too specific, due to a lack of concrete data available. VTC.

".. have a much higher intelligence than what you would expect if you linearly projected intelligence as a function of brain size." -- Then don't use a linear model.

It also may be the case that we are implying intelligence in some cases.
The responses these animals show may have been evolutionarily selected as it best for their survival. However, to us the benefits of these responses may not be directly visible. For example, sheep herding dogs may have a high degree of spatial and numerical capabilities since humans bred them for these traits.

I am not sure it answers the question. The question is about neurophysiology, not about evolutionary pressure or out potential bias to mis-estimate one species intelligence.

I think it is a valid point to keep in mind to explain some things, but you really can't use the rhetoric "it's just pure  instinct" to explain all the results without infringing upon other models or an accepted consensus in biology, at least not without precisely defining the exact mechanisms where this is proven to takes place across every species.

I agree with @RayOfHope that this is a valid point. Misinterpreting instinct as intelligence or considered behaviour would be critical when answering the question of size vs intelligence.

Implicit in the question is the assumption that the examples of the animals you mention somehow would outperform species (with brains) of similar size. Comparing intelligence between different species, no matter how you define it, is going to be challenging.
I would argue that it is impossible to devise a single task with which to compare such different species as ants, octopi, crows, and rats. However some correlations between cognitive capacity and some anatomical features of the brain have been investigated.
Brain-to-body mass ratio
The scaling of the ratio of total brain-to-body mass is not linear. It rather follows a power law relationship, typical to allometric scaling.
$$ m_{(brain)} = \alpha \times m_{(body)} ^R $$
It is convenient to log-transform the mass variables in order to work on the following linear relationship:
$$ log(m_{(brain)}) = R \times log(m_{(body)}) + log(\alpha) $$
The following plot from wikipedia displays this relationship for a number of different species. The slope of this line is $R$, and the intercept $log(\alpha)$. H. Jerrison proposed that the distance of a species from this line could provide an estimate of cognitive capacity. He called that measure encephalisation quotient. The reasoning behind this idea is that of course the brain of bigger animals will be bigger and that of small animals smaller, but is it bigger or smaller than expected from this simple universal model? If so, that may provide a clue for more advanced cognitive skills.

[CC BY-SA 4.0], via Wikimedia Commons
Indeed, we can see as examples that humans and dolphins diverge from this line quite distinctly, which matches with our intuition about these species' cognitive abilities, but so do some species of mice. Is this metric good enough to predict cognitive abilities overall? Given the primitive functions that many brain areas are associated with, such as the brainstem, it is not straightforward that a simple overall increase of brain size above what this simple model would predict, would confer any benefit to the overall cognitive capacity of an animal. At least when attempting to correlate cognitive capacity with several measures based on brain anatomy of non-human primates, it was found that overall (log)brain size or (log)neocortex size are better predictors than the encephalisation quotient. The proportion of brain volume that the neocortex occupies is also able to distinguish the brains of primates from those of insectivores or carnivores. Given the high-level functions that the neocortex is involved with, these results are not surprising.
Neuron size and density
Scaling of the whole brain or the neocortex can be due to a number of things. Either more cells are added, the cells become bigger, more glial cells are added etc. So which is it? According to a 2014 paper by the Kaas group more neurons are added in the cerebral cortex and the cerebellum. This results in a decrease in neuronal density in all species studied except primates, where neuronal density appears to remain relatively stable with the number of neurons. The authors conclude from this result that neuronal size (including axons and dendrites) must have remained stable in primates.

To answer your question, if we take overall brain size or neocortex size as a proxy for the cognitive capacity of an animal, we can conclude that the relationship indeed is not linear, as you predicted. However, we have no reason to believe that some species are exceptionally more endowed than what would be expected of them based on brain size given this non-linear relationship, except perhaps primates. Of course comparing mammals to invertebrates based on this evidence is a non-starter as they lack a centralised brain and/or neocortex.
Although we may be surprised by the remarkable things some species can do, this may only mean that we have not looked close enough at the capabilities of other yet unsuspected species. Conversely, our amazement may simply be because of the fact that we underestimate the capabilities of animals that are not similar to us.
Further reading: Evolution of the brain and intelligence, G. Roth and U. Dicke, TICS, 2005.10.1016/j.tics.2005.03.005
Related questions in Biology SE:

Is there a correlation between total neurons and intelligence?
Is the ratio Brain Mass/Total Mass still considered a valid indicator of intelligence?


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What kind of spider is this?(Rajasthan, India)

Hi there, I found this insect in India/Rajasthan. Is this a spider or scorpion? It was nearly 50 mm in length.

That's neither a spider nor a scorpion (and, of course, not an insect). That's a solifuge, a different group of Arachnida.
The most common Genus of solifugae in India is Galeodes, which resembles the specimen in your photo:

Genus Galeodes
However, narrowing it down to the Genus may be a little bit more complicated.
It's worth mentioning that, despite their frightening appearance, they are not dangerous to humans.


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What is this flying animal that hovers like a hummingbird?
What is this animal?

Characteristics:

Has a long curved bill.
Has green upper body and a dark black lower body.
Likes petunias.
Hovers like a hummingbird but is a bit smaller.
Has small rear feather-like tufts and is very odd shaped.
Moved quickly from flower to flower.

Yes, that's definitely a duplicate. I'm voting to close.

Also, I just turned my answer into a community wiki, so I don't get any more points for this answer.

That's a lepidopteran insect called hummingbird moth.
There are several species of hummingbird moths. Their more distinctive feature, as the name implies, is that they hover just like a hummingbird.
Your photo is not the best one for identification, but it seems to be a hummingbird hawk-moth, from the Genus Macroglossum, specially because the rear feather like tufts (which are just elongated setae).
Here is a better photo, for comparison:

Macroglossum stellatarum
However, according to the colors you described, your species is probably different from that in the photo above.
Here is one flying (from a different species):

Do you know the typical habitat. I was left puzzled during a visit to Lantau Island, Honk Kong and this looks similar.

It depends on the exact species.


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Are neurodegenerative diseases such as dementia inevitable?
For the sake of this question, let's imagine a person who lives to 200, would it be at all possible for them not to get dementia? Is it an inevitable disease as we get older or can it be avoided?

I won't think it becomes "inevitable" at 200...but yes, chances do increase, just like cancer

I think this is a great question but at this point it isn't really answerable without being substantially opinion-based.

To my knowledge the oldest verified human age is below 123 years (https://en.m.wikipedia.org/wiki/Oldest_people). To reach 200, revolutionary achievements are necessary. There is no telling, how these might change the probability of dementia occurring. I am afraid, any answer  is bound to be highly speculative.

While the chances do increase, the majority of people who make it past 100 don't suffer from dementia.

@jamesqf - There's a huge difference between 100 and 200. Also, the 'majority' is small, and gets smaller every half-decade. Rates (of dementia) increased exponentially with age from 12.7% per year in the 90–94-year age group, to 21.2% per year in the 95–99-year age group, to 40.7% per year in the 100+-year age group.. However, the answer is unknown and POB.

One of the best questions I have seen in a long time. It is very central in gerontolical research. I would argue that dementia would occur at somepoint, simply because more and more cells would be approaching the hayflick limit, leading to the inevitable loss of neurons at some stage.


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Plant-human hybrid?
I was bored on YouTube so I searched "plant-human hybrid" and this video came up https://www.youtube.com/watch?v=MiZ35pkxG-k. and I want to know if this is actually possible, I checked the comments but they where mostly weed jokes, so is this possible

Welcome to SE Biology. I would ask you to relieve your boredom by reading the guided tour and finding out what constitutes a suitable question. Questions should be comprehensible in themselves and not require one to follow a link to find them. You need to describe what was proposed in the film in your question. Otherwise it is likely to be closed.

This is already a common phenomenon in biotechnology. Perhaps it is exactly not what you think or saw in the video. By the way, in the video the plant was Mimosa pudica and the phenomenon was seismonastic movement...so a very misleading video.
Biotechnology already harnesses plant-non plant hybrids to be specific to produce transgenic plants which uses the useful genes from a different organism to produce a particular vitamin, drug, enzymes, etc in large amount.This phenomenon is called molecular farming and such hybrid plants act as bioreactors.
Similarly mouse genome segments may be used to produce antibody producing plants through their fruits or seeds. Brassica napus uses segments of DNA from Hirudinea organisms like leech to mass produce hirudin used in medicinal product.
It is quite similar to E. coli in which segments of human genes are introduced to mass produce insulin.The E. coli serves as a bioreactor in this case.
I'm mentioning only a few references which explains the detailed processes by which the entire plant cell is endowed with the special traits from other organisms.
FOR REFERENCE:https://www.ncbi.nlm.nih.gov/pubmed/9274048E
https://www.nature.com/nature/journal/v342/n6245/abs/342076a0.html
https://en.m.wikipedia.org/wiki/Genetically_modified_crops